Emergency Neurological Life Support, Protocols.2019.4th Ed

Emergency Neurological Life Support
Acute Ischemic Stroke Protocol

Version 4.0
Authors
Archana Hinduja, MD
Noah Grose, BSN, MSN, ACNP-BC
Deborah S. Tran, DNP, RN, CNRN, SCRN, NE-BC
Aaron Raleigh, BA, EMT-P
Last updated: October 2019
Protocol developed by: Noah Grose, BSN, MSN, ACNP-BC

Acute Ischemic Stroke Algorithm
(click each box for details)
Checklist & Communication

Acute Ischemic Stroke Table of Contents
Acute Ischemic Stroke Algorithm ...............................................................................................1

Checklist ...................................................................................................................................3
Communication .........................................................................................................................3
Acute Ischemic Stroke...............................................................................................................5
IV tPA Administration ................................................................................................................6
Once a patient is deemed a candidate for IV thrombolytics ...................................................6
Endovascular Treatment ...........................................................................................................7
Consider mechanical thrombectomy ......................................................................................7
Hospital Admit or Transfer .........................................................................................................8
While waiting for ICU bed ......................................................................................................8
Consider patient transfer if: ....................................................................................................9
Low Risk TIA ...........................................................................................................................10
ABCD2 Score 0-3 .................................................................................................................10
No tPA unless BP is reduced ..................................................................................................11
Blood pressure (BP) exceeds 185/110 mmHg .....................................................................11
High Risk TIA ..........................................................................................................................12
TIA risk moderate or high, or unable to arrange timely outpatient work-up and follow-up.....12
Onset Less Than 3 hours ........................................................................................................13
Time from stroke symptom onset is less than 3 hours .........................................................13
Onset Between 3 and 4.5 Hours .............................................................................................16
Time from stroke onset is between 3 and 4.5 hours .............................................................16
Patient improves following tPA ................................................................................................17
Measurable improvement within 1 hour? LVO Present or Suspected ..................................17
Yes - Patient is an IV tPA Candidate .......................................................................................18
Is Blood Pressure (BP) less than 185/110 mmHg? ..............................................................18
No: Patient is not an IV tPA or IA Treatment Candidate ..........................................................19
Neither IV tPA or Endovascular intervention is appropriate ..................................................19
Symptom Onset > 4.5 hours ....................................................................................................20
Outside IV tPA window ........................................................................................................20
The ABCD2 Score ...................................................................................................................21
What is the predicted risk for stroke? ...................................................................................21
TIA ..........................................................................................................................................22
Symptoms have completely resolved ...................................................................................22
2
Checklist
☐ Activate stroke code system (if available)
☐ Vital signs
☐ Supplemental oxygen to maintain saturation ≥ 94%
☐ Determine time of onset / last known well time (LKW)
☐ Determine NIHSS score
☐ CT, CTA
☐ Medication list*
☐ IV access - 18g peripheral IV
☐ Labs: Fingerstick glucose, CBC with platelets, PT/ INR, PTT, and beta-HCG for women of
childbearing age
☐ EKG
*When asking about medications, be sure to ask specifically about anticoagulants and when
medication was last taken/administered.
Communication
☐ Age
☐ Airway status
☐ Last known well time (LKW)
☐ NIHSS
☐ Coagulation parameters – PT, PTT, INR
☐ CT – Dense MCA sign, MCA dot sign, dense basilar sign, ASPECTS score, early ischemic
changes
☐ CTA/MRA – Large vessel occlusion (ICA, M1, M2, Basilar, PCA)
☐ CTP – Volume of core and penumbra, matched or mismatched perfusion
☐ Thrombolytic administration – yes (Initiation, completion time); no (reason)
☐ Endovascular intervention (time to groin puncture, recanalization, TICI score)
☐ Target BP
Sample Sign-Off Narratives

Prehospital to ER:
“I am signing out a 62 yo male with known hypertension and atrial fibrillation who is not on
anticoagulation”.
“He was found down on the floor at 7:10 am by his wife. He was last seen normal at 10 pm last
night. He is aphasic with right-sided weakness, GCS of 11, HR of 130/minute and BP of
3
200/110 mmHg. IV Metoprolol 5 mg given and his follow up HR was 94/minute and BP was
182/90 mmHg”
ER to ICU:
“Upon arrival to the ER at 9:10 am his NIHSS was 21 - global aphasia, left gaze preference,
right hemiplegia and neglect.”
“CT completed at 9:26 am showed a left dense MCA sign. CTA showed a left M1 occlusion.
CTP showed a core of 38 ml, penumbra of 140 ml, mismatch volume 102 ml, mismatch ratio
3.7.”
“He was out of the IV tPA window. Endovascular team was notified at 9:38 am”.
“He was taken to the cath lab at 9:50 am. His HR was 106/minute and BP was 190/106 mmHg.
Groin puncture was attained at 10:06 am. TICI3 revascularization was achieved. He had
started moving his right arm and leg few minutes after the procedure”.
“His target post procedural BP should be <140/80 mmHg”. MRI brain is pending”.
4
Acute Ischemic Stroke

Acute ischemic stroke (AIS) is a neurological emergency that can be treated with time-
sensitive interventions, including both intravenous thrombolysis and endovascular approaches
for thrombus removal. Numerous studies have demonstrated that rapid, protocolized
assessment and treatment is essential to improving neurological outcomes. These
interventions are often completed simultaneously to achieve a safe and fast medical and/or
surgical intervention. The protocol focuses on the early identification and initial management,
within the first hour(s) following acute onset of a neurological deficit.
5
IV tPA Administration
Once a patient is deemed a candidate for IV thrombolytics
After placing two peripheral IV lines:

• Weigh the patient; do not estimate body weight. If patient cannot be weighed, then
two people should estimate weight.
• Mix by swirling (do not shake) 0.9 mg/kg tPA, total dose not to exceed 90 mg.
• Give 10% of the total dose of tPA by bolus over 1 minute, then infuse the remaining
dose over 1 hour.
• The remaining tPA in the IV tubing at the end of the infusion should be administered
by running an additional 100 ml of saline at the same rate of the tPA infusion until
the line is cleared.
Alternative dosing strategies utilizing lower doses has been evaluated in the literature;
however, currently these dosing strategies are not endorsed by the AHA/ASA guidelines and
should not be routinely implemented.
Footnote:
As tPA is dispensed in 50 and 100 mg bottles, it is suggested to withdraw and discard any
excess tPA from the vial to avoid accidental infusion of excess tPA.
6
Endovascular Treatment
Consider mechanical thrombectomy
Mechanical thrombectomy should be considered if the patient has a large vessel occlusion
(proximal (M1) MCA, intracranial ICA, basilar or vertebral artery) and is within a 24-hour time
window of last know well time. If the patient is a candidate for IV thrombolytics, it should be
administered expeditiously, regardless of endovascular procedure candidacy.
Large vessel occlusion can be suspected by seeing a hyperdense sign (clot within the vessel)
on non-contrast CT imaging but this sign is insensitive. The probability of a large vessel
occlusion increases with NIHSS score. An NIHSS >6 should raise suspicion for a large vessel
occlusion. CTA or MRA is diagnostic, as is conventional angiography.
• Contact the neurointerventional physician on call; if the treating hospital does not
have this capability, consider transfer to a comprehensive stroke center
• Based on the results of DAWN and DEFUSE 3 Trials, mechanical thrombectomy
should be considered based on CTP, DWI – MRI + MRI perfusion is recommended
to aid in the selection of patients for mechanical thrombectomy who meet the
eligibility criteria
7
Hospital Admit or Transfer

While waiting for ICU bed
After IV, endovascular intervention or no specific treatment consider the following initial
admission orders:
• Neuro check every 15 min for 2 hours, then every 30 minutes for 6 hours, then
hourly
• Oxygenation to keep O2 sat > 94%
• Blood pressure (BP) check every 15 min for 2 hours, then every 30 minutes for 6
hours, then every hour for 16 hours
• After IV tPA thrombolysis maintain BP <180/105 mmHg (note: this is lower than
pretreatment values); if no tPA given, keep BP < 220/120 mmHg
• Bedside swallow test is quickly performed by giving 30 ml water by mouth.
Dysphagia screening should be performed before administering anything else orally.
Certain stroke patients are at high risk of aspirating. If the patient coughs or chokes
during the bedside swallow test, then they should remain NPO until additional formal
testing can be performed
• Keep glucose 140-180 mg/dl, consider insulin drip if blood glucose is persistently >
200 mg /dl.
• IVF (normal saline) at 1.5 ml/kg/hour to keep euvolemia
• Monitor for A-fib for at least 72 hours after admission
• Monitor for and prevent fever. Fever is detrimental to already injured brain. Treat
fever sources with antibiotics or therapies while preventing fever with antipyretics.
Rectal or IV acetaminophen or IV ketorolac will help control fever. Therapeutic
hypothermia has not been proven effective to improve clinical outcome after acute
stroke.
• Avoid indwelling urinary catheter to avoid nosocomial infection
• For large cerebral infarctions, it may be prudent to keep the head of bed elevated 30
degrees to help reduce edema. Decompressive surgery (including prophylactically)
is recommended in some patients with malignant edema who have/to prevent
sudden deterioration due to herniation from this massive swelling.
If tPA was administered:

• Avoid inserting urinary catheter, nasogastric tubes (NGT), intra-arterial (IA)
catheters. If absolutely needed avoid insertion of urinary catheter during tPA
infusion and at least 4 hours afterward. NGT and IV catheters should be avoided
for 24 hours. Do not give anticoagulant/antiplatelet therapy for 24 hours; repeat
head CT or MRI at 24 hours before starting anticoagulant/antiplatelet medications
Watch for complications of tPA, including

• Angioedema – with potential for airway obstruction. Most will treat just as an allergic
reaction with
o H-1 blockers, e.g. diphenhydramine 50 mg IV
o H-2 blockers, e.g. ranitidine 50 mg IV, and
8
o Steroids, e.g. methylprednisolone 125 mg IV

o Epinephrine 0.3 mg subcutaneously or via nebulizer
o Icatibant (bradykinin antagonist) 30 mg sub cutaneous in abdominal wall, repeat
in 6 hours, and maximum of 90 mg in 24 hours
o FFP (contains C1 esterase inhibitor) may be required as targeted therapy for
hereditary angioedema and ACEI-related angioedema.
o Consider early/rapid intubation if there are early signs of airway compromise. It
is typically not necessary if there is only isolated lip or tip of tongue swelling.
• Hemorrhage - stop tPA
• Sudden deterioration in mental status - see below
• Severe hypertension or hypotension - may be signs of ICH or systemic hemorrhage
A sudden decline in neurological exam during or following tPA administration may be due to an
intracranial hemorrhage. This is often accompanied by a marked rise in blood pressure;
however, a marked rise or fall in blood pressure alone may signal an ICH. Do the following
immediately:
• STOP tPA infusion
• Monitor airway closely
• Vital signs every 15 minutes (assessment for signs of increased ICP). Assess
GCS/pupil response. Treat blood pressure and use noninvasive interventions to
lower ICP (raise HOB, neck midline).
• Obtain STAT head CT scan
• Notify your neurosurgeon on call; if not available begin the process to transfer the
patient to a facility with neurosurgical capability if the CT scan shows hemorrhage
• Stat labs: PT, PTT, Platelets, fibrinogen, type and cross 2-4 unit PRBCs
• Give the following:
o 10 units of cryoprecipitate IV over 10-30 min. Give more until fibrinogen level
<200 mg/dL
o And
▪ Tranexamic acid 1000 mg IV over 10 min or
▪ Aminocaproic acid IV 4-5 g over 1 hour followed by 1 g until bleeding
stops (usually within 3 hours)
o Consider transfusion of 1 bag of single donor platelets or 6 to 8 bags of random
donor platelets.
Consider patient transfer if:
• the treating hospital cannot provide the level of care for the patient (no ICU for
example). Patient outcomes have been shown to improve if the patient is treated in a
stroke center.
• there is suspicion of large vessel occlusion (CTA/MRA, hyperdense vessel sign on
imaging; or clinical findings consistent with an MCA stroke) and the patient can
arrive and be treated at the receiving hospital within 24 hours of symptom onset.
9
Low Risk TIA

ABCD2 Score 0-3
Patients at low risk of stroke can be treated as outpatients. This can begin in the ED or clinic
starting with medications and expediting ECG and imaging of the carotids in 1-2 days following
the ABCD2 score calculation. Do the following:
• Start on antithrombotic agent (ASA 81 mg/day, clopidogrel 75 mg/day, or ASA/
extended release dipyridamole 200 mg twice daily)
• Initiate high intensity statin if not taking one already (moderate intensity statin in
patients > 75 years old)
• Obtain a 12-lead ECG or review the rhythm strip if available. If these show atrial
fibrillation, consider starting anticoagulation (oral anticoagulant or low molecular
weight heparin) or ASA 81 mg if anticoagulation is contraindicated; calculate
CHADS2 or CHADS2Vasc and HAS-BLED score to help guide long term therapy.
• Consider initiating longer-term outpatient cardiac monitoring (30 days) if the TIA is
embolic and atrial fibrillation is not identified already or if there is no other cause for
TIA
• Arrange carotid imaging: ultrasound, CTA or MRA
• Consider transthoracic echocardiography
• Initiate smoking cessation counseling
• Counsel about the importance of compliance with medication regimen
10
No tPA unless BP is reduced

If the patient is a potential thrombolysis candidate, interventions to control BP should be
initiated immediately. Short-acting intravenous and/or titratable IV antihypertensive agents can
be used for the treatment of hypertension in the acute setting.
Blood pressure (BP) exceeds 185/110 mmHg
• This is too high for IV tPA administration and requires gentle reduction prior to
initiating tPA.
• Labetalol 10-20 mg IV every 10 minutes (consider doubling dose (i.e. 20 mg, 40 mg,
80 mg) to maximum total dose of 300 mg. Start maintenance infusion.*
• Nicardipine IV- start 5 mg/hour, titrate up by 2.5 mg/hour at 5- to 15-minute intervals,
maximum dose 15 mg/hour; when desired blood pressure attained, lower the dose.
• Clevidipine IV- begin with 1-2 mg/hour IV infusion; double medication dose every 90
seconds until BP goal is neared, then increase in smaller increments until desired
BP goal is reached. Maximum dose is 32 mg/hour.
• Other medications. **
If BP falls below 185/110 mmHg, proceed to IV tPA administration.
If BP proves refractory to the above, the risk for intracerebral hemorrhage is considered too
high and the patient should not be treated with tPA. Continue to treat BP to keep less than
220/120 mmHg, however. ***
Footnotes:
*Be sure to initiate a continuous infusion of the antihypertensive agent as boluses will wear off
and BP will likely return to its previous high levels.
**Nitroglycerin paste (for patients with no IV access), labetalol, and nicardipine are
recommended by the American Stroke Association. See ENLS: Pharmacotherapy.
***Permissive hypertension is allowed for TIA, as it is for non-tPA treated patients, up to

220/120 mmHg. This may be gradually lowered over the next 24-48 hours.
11
High Risk TIA

TIA risk moderate or high, or unable to arrange timely outpatient work-up and
follow-up
Admit for observation:

• Patients with an ABCD2 scores > 3
• Permissive hypertension (not to exceed 220/120 mmHg), and BP should be
gradually lowered over 24-48 hours.
• Keeping head of bed flat for 24 hours has been recommended in the past but is not
evidence-based.
• Telemetry
• In a high risk TIA (ABCD2 score ≥ 4) the CHANCE trial demonstrated that dual
antiplatelet therapy using a combination of clopidogrel (initial dose of 300 mg
followed by 75 mg/day) and aspirin 81 mg/day for 21 days followed by clopidogrel 75
mg/day for 90 days was superior to aspirin alone in reducing the risk of stroke.
• Similarly, the POINT trial from United States showed that combined use of
clopidogrel at a loading dose of 600 mg once followed by 75 mg/day for 90 days plus
aspirin 50-325 mg/day for first 21 days was superior to aspirin 50-325 mg/day for 90
day. Initiate high intensity statin if not taking one already (moderate intensity statin in
patients > 75 years old).
• Initiate high intensity statins (ex: atorvastatin 80 mg daily or rosuvastatin 20 mg
daily)
• Obtain a 12-lead ECG or review the rhythm strip if available. If these show atrial
fibrillation, consider starting anticoagulation (oral anticoagulant or low molecular
weight heparin) or ASA 81 mg if anticoagulation is contraindicated; calculate
CHADS2 or CHADS2Vasc and HAS-BLED score to help guide long term therapy.
• Consider initiating longer-term outpatient cardiac monitoring (30 days) if the TIA is
embolic and atrial fibrillation is not identified already or if there is no other cause for
TIA.
• Arrange carotid imaging: ultrasound, CTA or MRA
• Consider transthoracic echocardiography
• Initiate smoking cessation counseling
12
Onset Less Than 3 hours

One of the chief criteria used to select patients for acute stroke interventions is the patient’s
time of stroke onset defined as LKW time or alternatively the time of symptom onset (if
witnessed). Acute stroke treatment therapies such as thrombolysis are time sensitive, and
delays can lead to a lower likelihood of a good outcome and an increased risk of intracranial
hemorrhage. If you cannot establish the time with certainty, most providers will not treat with
IV tPA.
Time from stroke symptom onset is less than 3 hours
Time of onset is when the patient was last seen normal.

• If patient or observer can verify when the first symptoms began, use that time.
• If a patient awakens with a stroke, the time of onset is when they last went to bed.
Patients with a shorter time to tPA administration have a higher likelihood of good outcome.
Therefore, expediting care may greatly impact your patient.
Check eligibility for on-label (US and elsewhere) use of IV tPA:

• Diagnosis of ischemic stroke causing measurable neurological deficit. Tip: ask the
patient if the deficit is disabling to them - can they carry out all of their normal and
enjoyable activities as they could before this event?
• Onset less than 3 hours before initiating tPA
• Patient is at least 18 years of age (see section on Pediatric Stroke)
Alteplase is the only FDA-approved tPA for use in acute ischemic stroke in the U.S. However,
the 2018 AHA/ASA Acute Ischemic Stroke Guidelines now give tenecteplase 0.4 mg/kg single
IV bolus a class 2b recommendation as an alternate medication.
Absolute Exclusion Criteria if positive:

Most clinicians practice using a hybrid of AHA/ASA and FDA guidelines. Be aware that
FDA lifting of restrictions is based on there being no study that has specifically validated a
particular parameter. Previous guidelines were extensions based on the exclusion criteria
under which the medication was originally trialed.
• The symptoms of stroke should not be suggestive of subarachnoid hemorrhage.
(2015 FDA label, changed to subarachnoid hemorrhage)
• No major head trauma in previous 3 months
• No prior stroke within previous 3 months (removed in 2015 FDA label)
• No intracranial or intraspinal surgery in the previous 3 months
• No arterial puncture at a non-compressible site or lumbar puncture in the previous 7
days
• No history of previous intracranial hemorrhage (contraindication removed in 2015
FDA label, warning added for recent ICH)
13
• No history of intracranial neoplasm, aneurysm, or arteriovenous malformation. Note

that it is probably prudent to give IV tPA to a patient with an ischemic stroke and a
small asymptomatic, unsecured intracranial aneurysm.
• Blood pressure not elevated (systolic < 185 mmHg and diastolic < 110 mmHg) (in
2015 FDA label, specific BP values removed from contraindication, warning for BP >
185/110 mmHg remains)
• No evidence of active bleeding or acute trauma (fracture) on examination.
• Not taking an oral anticoagulant or, if anticoagulant being taken, INR < 1.7 or PT >
15 seconds.
• No current use of direct thrombin inhibitors or direct factor Xa inhibitors or elevated
sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT (ecarin
clotting time); TT (thrombin time); or appropriate factor Xa assays *
• If receiving heparin in previous 48 hours, aPTT must be in normal range.
• Platelet count <100 000 mm3.
• Blood glucose concentration < 50 mg/dl (2.7 mmol/l) **(FDA 2015 label, removed
entirely). In spite of the FDA removal of limitation, a blood glucose test (serum or
capillary) is the only test result one should have back before administering tPA.
• CT does not show a multilobar infarction (hypodensity >1/3 cerebral hemisphere)
(removed from FDA 2015 label)
Relative Exclusion Criteria if positive:

Use caution in recommending tPA if one or more are positive:
• The neurological signs are rapidly improving ***(removed from 2015 FDA label)
• The neurological signs are minor and isolated ****(removed from 2015 FDA label)
• Pregnancy
• Seizure with postictal residual neurological impairments
• Major surgery or major trauma in the previous 14 days
• Gastrointestinal or urinary tract hemorrhage in previous 21 days
• Myocardial infarction in the previous 3 months
Some additional considerations:

• Caution should be exercised in treating a patient with major deficits.
• Caution using tPA in patients treated with low molecular weight (LMW) heparin in the
past 24 hours. Note that prophylactic dose of LMW heparin is NOT a
contraindication, only the full treatment dose.
• The patient or family members understand the potential risks and benefits from
treatment. No written consent is required but the conversation should be
documented in the clinical notes. Do not delay therapy if surrogate is not available.
* Novel new direct thrombin inhibitors or direct factor Xa inhibitors pose a new conundrum
in determining tPA eligibility. Without available blood tests and based on drug half-lives, most
14
practitioners are using a cut-off of 48 hours (or 5 half-lives) since last use of any of these
medications before recommending tPA.
** The original tPA guidelines for acute ischemic stroke included an exclusion for patients
with serum or capillary glucose level > 400 gm/dl. While this parameter has been removed for
many years, a level this high should prompt the consideration of an alternate diagnosis.
Similarly, a low blood glucose level may be symptomatic and should be corrected and the
patient’s neurologic status be reassessed.
*** Some stroke patients will have stuttering symptoms or they may have mild improvement,
e.g. from a NIHSS of 12 to 8 points, but then hold at 8 with no further improvement. The
recommendation is to still treat these patients.
**** In the past, many physicians used an NIHSS of 4 or 5 points as a lower end cut-off for
recommending tPA. It must be noted that patients may have significant residual stroke
symptoms with low NIHSS scores (e.g. isolate hemianopsia, or aphasia, or brain stem injury).
tPA administration should strongly be considered in these patients. Asking the patient about
how disabling their symptoms are will help with the tPA recommendation.
15
Onset Between 3 and 4.5 Hours

Time from stroke onset is between 3 and 4.5 hours
Time of onset is when the patient was last seen normal.

• If the patient or an observer can corroborate when the first symptoms began, use
that time.
• If a patient awakens with a stroke, the time of onset is when they last went to bed.
The time of onset is critical for using tPA as the risk of intracerebral bleeding increases with
increased time from stroke onset. If you cannot establish the time with certainty, most
physicians will not treat with tPA.
In the US, tPA is not yet FDA approved for 3- 4.5-hour time window, although it is approved in
Europe and Canada. Nonetheless, the 3- 4.5-hour window is endorsed by the American Heart
and American Stroke Association. The inclusion criteria are similar to those of < 3 hours, but
are modified as follows:
• Meet all criteria of < 3 hours since stroke onset

• Age < 80 years
• No anticoagulant use, regardless of INR
• NIHSS < /= 25
• No combined history of prior stroke and diabetes
16
Patient improves following tPA

Measurable improvement within 1 hour? LVO Present or Suspected
Often this is defined as a lowering of the NIHSS score, and there is no clear consensus as to
how much. If the patient is suspected or confirmed to have a LVO, begin working on getting
the patient to an endovascular center for evaluation right away.
17
Yes - Patient is an IV tPA Candidate

Is Blood Pressure (BP) less than 185/110 mmHg?
After reviewing the inclusion/exclusion criteria for IV tPA use, the patient is eligible to receive
the drug. Current blood pressure is the last inclusion criteria.
Blood pressure (BP) measurements are vital and must be obtained frequently, especially in the
early management of AIS. If the patient is a potential thrombolysis candidate, interventions to
control BP should be initiated immediately. Target BP goals for patients eligible for IV tPA is <
185/110 mmHg, and once IV tPA is initiated, BP must be maintained below 180/105 mmHg for
24 hours after administration of IV tPA to limit the risk of intracranial hemorrhage. A strategy
for careful BP lowering should be employed while ensuring large fluctuations in BP once at
goal are limited.
Steps can be taken to lower blood pressure so as to make the patient eligible for tPA. See the
ENLS: Pharmacotherapy protocol for dosing. Note that while the FDA has lifted absolute target
BP numbers, the AHA/ASA guidelines still recommend getting and keeping BP down below
185/110 to start tPA and even lower below 180/105 while tPA is infusing
18
No - Patient is not an IV tPA or IA Treatment Candidate

Neither IV tPA or endovascular intervention is appropriate
Common exclusions for IV tPA are time (duration > 4.5 hours) or specific contraindications to
tPA.
Endovascular intervention exclusions include lack of large vessel occlusion on CTA or MRA,
large area of infarction already present on the brain imaging study (ASPECTS score < 6).
CTA/CTP or MRI/MRA may show large infarct core and small penumbra indicating that
endovascular intervention will not be successful and may in fact be dangerous.
19
Symptom Onset > 4.5 hours

Outside IV tPA window
Beyond 4.5 hours, IV tPA is associated with increased risks and unproven efficacy.
Endovascular therapies are often helpful in this time window (and earlier as well) if there is a
LVO.
20
The ABCD2 Score

What is the predicted risk for stroke?
The ABCD2 score is an ordinal scale that provides risk prediction of stroke following the TIA. It
is scored as follows:
ABCD2 Element Points

Age > 60 years 1
Blood pressure ≥ 140/90 mmHg on initial 1
evaluation
Clinical features
Speech disturbance without weakness 1
Unilateral weakness 2
Duration of symptoms
10 - 59 minutes 1
60 minutes or greater 2
Diabetes mellitus in patient’s history 1
Total score 0-7
The following is the estimated risk (%) of a stroke occurring within various time ranges:
Total risk ABCD2 Score 2 day 7 day 90 day

Low 0-3 1.0 1.2 3.1
Moderate 4-5 4.1 5.9 9.8
High 6-7 8.1 12 18
Ref: Cucchiara B et al, Ann Emerg Med 2008, 52:S27-39
Based on this risk stratification, some physicians choose to admit high-risk patients and
discharge those with low risk, and controversy exists about moderate-risk patients.
21
TIA
Symptoms have completely resolved
Diagnosis of TIA (transient ischemic attack) is based on new onset of focal neurological
symptoms that are explainable by a vascular cause (i.e. arterial occlusion of a single or group
of arteries adequately explain the patient's signs and symptoms) and these signs and
symptoms resolve within 24 hours (most TIA’s resolve in a much shorter period of time). If the
patient’s symptoms clear by 24 hours but an acute infarct is observed on brain imaging, this is
defined as a stroke and no longer TIA.
22
Airway, Ventilation and Sedation Protocol
Version 4.0
Authors
Asma Moheet, MD, FNCS
Marlina E. Lovett, MD
Stephanie Qualls, RN, BSN, CNRN
Venkatakrishna Rajajee, MBBS
Protocol developed by: Venkatakrishna Rajajee, MBBS

Airway, Ventilation and Sedation Algorithm
Checklist and Communication

Checklist
□ Assess the need for intubation or noninvasive positive pressure ventilation
□ Perform and document a focused neurological assessment prior to intubation
□ Verify the endotracheal tube position
□ Determine ventilation and oxygenation targets, and verify with ABG/SpO2/ETCO2
□ Assess the need for analgesia and/or sedation in mechanically ventilated patients
Communication
□ Mental status and neurological examination immediately pre-intubation
□ Intracerebral hemorrhage (ICH) score, if appropriate
□ Vitals, hemodynamics, and gas exchange pre- and post-intubation
□ Relevant drugs used around intubation
□ Technique of intubation, confirmation of tube position
□ Ease of bag mask ventilation, intubation, and tube passage
□ Cormack–Lehane grade, if appropriate
□ Ventilator settings, ventilation, and ETCO2 targets
□ Analgesia and sedation strategy
□ Pending investigations
Sample communication:
“Mr. Smith, 52-year-old gentleman with intracerebral hemorrhage required urgent intubation.”
“His GCS was 6 prior to intubation—would not open eyes to pain, was mute, and would only
withdraw to pain on the right; he appeared to be left hemiplegic. His right pupil was 5 mm and
sluggish, and left pupil was 3 mm and briskly reactive. Following intubation, his pupils are
3 mm and reactive bilaterally.”
“His vitals prior to intubation were BP 220/110, HR 66/m, SpO2 97% on 2 L/m nasal cannula.
Following intubation, his BP is 130/60, HR 55/m, SpO2 99% on FiO2 100% and ETCO2 is 32.”
“We treated with him with lidocaine, fentanyl, and 30 cc of 23.4% NaCL prior to intubation. We
used etomidate and rocuronium for RSI.”
“We intubated him with direct laryngoscopy using a Mac 4 blade. Tube position was confirmed
with a CO2 detector and auscultation.”
“Bag mask ventilation was easy, although I did use an oral airway. I had a Grade 2a view
without cricoid pressure, and tube passage was easy.”
“We have him on assist control, volume control, with a tidal volume of 6 cc/kg, respiratory rate
of 24/m, PEEP 5, and FiO2 100%. Our goal ETCO2 is 30–35, and goal SpO2 is > 94%.”
“We started a propofol infusion, titrated to deep sedation because of the herniation syndrome.”
“He will be transported to CT now, and the neurosurgeons will likely take him straight to the
operating room. We did not have time to get a chest X-ray, but he has equal breath sounds
and is ventilating and oxygenating well.”
“His wife is with him and has been counseled about his condition”
3
Airway, Ventilation, Sedation
Neurocritically ill patients often have evolving processes that threaten the airway and adequate
ventilation; as such, airway and respiratory management are of utmost importance. Airway
management, intubation, ventilation, and sedative choices directly affect brain physiology and
perfusion. Emergency Neurologic Life Support (ENLS) topics discussed here include acute
airway management, indications for intubation with special attention to hemodynamics and
preservation of cerebral blood flow, initiation of mechanical ventilation, and the use of sedative
agents based on the patient’s neurological status in the setting of acute neurologic injury.
4
Intubation - does the patient need to be intubated?

There are four commonly accepted indications to intubate a patient:
1. Failure to oxygenate
This finding may be determined by visual inspection such as evidence of respiratory
distress or cyanosis, vital signs data such as low oxygen saturation on pulse oximetry,
or laboratory data such as arterial blood gas analysis.
2. Failure to ventilate
Ventilation is assessed by visual inspection including observation of respiratory effort
exerted, capnometry through nasal cannula or transcutaneous monitoring [1], and/or
arterial blood gas analysis.
3. Failure to protect the airway
Airway protection is the result of numerous variables including bulbar function, airway
anatomy, quantity and quality of secretions, strength of cough reflex, and ability to
swallow after suctioning.[2, 3] The presence of a gag reflex is an inadequate method of
assessing airway protection.[4]
4. Anticipated neurological or cardiopulmonary decline requiring transport or
immediate treatment
Anticipation of the trajectory of the patient’s condition can allow for appropriate
preparation for the procedure as opposed to rushed or emergent intubations.
5
Document focused neurological assessment

Before sedatives/paralytics administered
Whenever possible, urgent management of the airway should coincide with a focused
neurological exam that may be conducted in 2 minutes or less. Document the neurological
exam in the record. This is an important baseline for subsequent care and is essential prior to
sedation or chemical paralysis.
Exam should include:

• Level of arousal, interaction, and orientation, as well simple cortical functions such
as vision, attention, and speech comprehension and fluency
• Cranial nerve function
• Motor function of each individual extremity
• Tone and reflexes
• Sensory level in patients with suspected spinal cord injury
• Involuntary movements such as tremor or seizure
• Cervical tenderness or gross spinal abnormality
6
Airway assessment
Assess for difficult bag-mask ventilation and intubation.
A difficult airway may be broadly defined as an endotracheal intubation attempt in which a

provider who is appropriately trained in airway management experiences difficulty with bag-
mask ventilation, tracheal intubations or both.
The "MOANS" mnemonic helps predicts ease of bag-mask ventilation:

M = Mask seal; may be compromised by abnormal facies, facial hair
O = Obesity / Obstruction (e.g. 3rd trimester pregnancy, neck swelling, angioedema,
hematomas, cancer)
A = Age > 55 years
N = No teeth
S = Stiff lungs
The "LEMON" mnemonic helps to predict difficult tracheal intubations:

L = Look for abnormal external facial features and body habitus
E = Evaluate the mouth opening and airway position using the 3-3-2 rule
• 3 fingers in open mouth between incisors
• 3 fingers between chin (mentum) and hyoid
• 2 fingers between hyoid and superior thyroid notch
M = Mallampati score
• Grade I- Soft palate, entire uvula, faucial pillars visible
• Grade II- Soft palate, entire uvula visible
• Grade III- Soft palate, base of uvula visible
• Grade IV- Only hard palate visible
O = Obstruction/obesity
N = Neck mobility
7
Pre-intubation checklist
PATIENT EQUIPMENT TEAM
1. RELIABLE IV/ IO ACCESS 1. MONITORING 1. ASSIGN ROLES

2. OPTIMAL POSITION o SpO2 with volume turned o First intubator
o Head of bed- consider up o Backup intubator
30-45o elevation o Quantitative waveform o Bag-mask ventilation
o Bed height capnography (ETCO2) o Manual in-line stabilization
o Access to airway o Electrocardiogram o Drugs
o Sniffing/ neutral Blood pressure- cuff to o Monitoring
cycle every 2 minutes or o Documentation
3. PRE-OXYGENATION arterial line. Cuff not on o Invasive airway
o Heated high flow nasal side of SpO2 probe. •
cannula 60-70 L/mt 2. Who will be called for
o Noninvasive positive 2. EQUIPMENT backup?
Pressure ventilation o Laryngoscope handle and
o Reservoir-bag mask blades, test bulb
o Bag-valve mask o Video laryngoscope, blade PLAN FOR DIFFICULTY
and rigid stylet
4. APNEIC OXYGENATION o Endotracheal tube x2 with 1. CANNOT INTUBATE CAN
IN PLACE stylet- selected size and VENTILATE
o Heated high flow nasal smaller option o 2-3 attempts by
cannula 60-70 L/mt o Bougie experienced operator with
o Nasal cannula 15L/mt o Oral/ nasal airway apneic oxygenation as
o Suction long as SpO2>95%
5. OPTIMIZE PATIENT o CO2 detector o Supraglottic airway
STATE o Supraglottic airway o Invasive airway
o Pre-treat with fentanyl and o Kit for invasive airway
lidocaine 2. CANNOT INTUBATE
o Raised intracranial 3. MEDICATIONS CANNOT VENTILATE
pressure- 23.4% NaCL or o Sedative o Supraglottic airway
mannitol o Neuromuscular blocking o Emergent
o Hypotension/ hypovolemia- agent Cricothyroidotomy
fluid bolus, vasopressors o Vasopressor
infusing o Sedation/ analgesia
o Left/ right ventricular failure- following intubation
vasopressor available/
infusing
8
Algorithm for endotracheal intubation
9
Intubation Sequence for Elevated ICP
10
Post-Intubation Checklist
 Secure endotracheal tube
 Confirm tube position, order chest x-ray
 Set cuff pressure to 20-30 cmH2O
 Pulse oximetry and quantitative waveform capnography
 Arterial blood gas measurement
 Deep sedation while neuromuscular blockade in effect
 Counsel next of kin on change in patient status
11
Goals of mechanical ventilation

Mechanical ventilation must be carefully titrated to maintain physiologic homeostasis as PaCO2
is a potent acute mediator of cerebral vascular tone and cerebral blood flow. Hyperventilation
to a low PaCO2 and high pH may cause decreased cerebral blood flow, worsening brain
ischemia. Hypoventilation to a high PaCO2 and low pH may cause cerebral vasodilation and
worsen intracranial hypertension. Hypoxia is an important cause of secondary brain injury,
while hyperoxia may also be harmful.
Immediately following intubation, respiratory and hemodynamic homeostasis should be

restored. The goals of mechanical ventilation are:
• Normalization of oxygenation utilizing the lowest FiO2 that will maintain oxygen
saturation of hemoglobin > 94%
• Normalization of ventilation to achieve a systemic pH of 7.35–7.45, and PaCO2 to 35–
45 mmHg (4.7 – 6.0 kPa) or ETCO2 that corresponds to PaCO2 target
• Therapeutic hyperventilation ONLY in the setting of cerebral herniation
• Normalization of the work of breathing
• Prevention of ventilator induced lung injury, using tidal volumes of 6-8cc/kg ideal body
weight and positive end-expiratory pressure (PEEP) ≥ 5.
• Management of ventilator-patient dyssynchrony.
Ideal Body Weight:

Men - 50 kg + 2.3 kg for every inch > 60 inches height (or every 2.54 cm above 152 cm)
Women - 45.5 kg + 2.3 kg for every inch > 60 inches height (or every 2.54 cm above 152 cm)
Oxygenation Goal: PaO2 > 110 mmHg, or SpO2 >94%, or disease specific goal.
12
Sedation
The goal of analgesia and sedation in the critically ill patient with neurological illness is to use
the lowest dose of sedative/ analgesic that maintains comfort and ventilator-patient synchrony,
while avoiding over-sedation and preserving the ability to clinically assess the patient’s
neurological status.
Occasionally, severe intracranial hypertension, status epilepticus, or the need for

neuromuscular blockade may necessitate a state of deep, continuous sedation..
• Titrate to light sedation using a validated sedation scoring system- Richmond Agitation-
Sedation Scale (RASS) 0 to -2 or Riker Sedation Agitation Scale (SAS) 3 to 4).
• Consider starting with analgosedation, using a short acting opioid infusion.
• Consider intermittent sedation.
• Dexmedetomidine or Propofol are preferred when continuous sedation is necessary.
• Deep sedation is necessary when neuromuscular blocking agents are used, in the
presence of intracranial hypertension refractory to light sedation, and the managmenet
of seizures refractory to other antiseizure therapy.
• Perform daily sedation interruption unless contraindications exist (e.g. high ICP, status
epilepticus).
• Employ non-pharmacological strategies: attention to day/night sleep cycles, limit noise,
play music as appropriate, reassuring presence of family and friends.
13
Commonly used sedative and analgesic agents in the
neurocritical care unit
Fentanyl: Fentanyl is an opioid agonist exhibiting analgesic effects with a rapid onset and
a short duration of action. It is an agent which can be used for analgosedation, or in
combination with a sedative.
Propofol: The lipid formulation of propofol allows for rapid penetration of the blood brain
barrier, resulting in rapid onset and cessation of action. It has potent and immediate
depressant effects on cerebral electrical and metabolic activity, and does not require renal
or hepatic metabolism for elimination. Disadvantages include robust vasodilating and
hypotensive effects, considerable IV lipid load, and the potential for the rare, but frequently
fatal, propofol infusion syndrome.
Benzodiazepines: Midazolam has a rapid onset of action and short duration of effect with
bolus administration, making it an ideal agent for procedural sedation. Bolus-dose
midazolam is a good choice for intermittent agitation in a NCCU population. Conversely,
midazolam infusions have been associated with prolonged mechanical ventilation.
Dexmedetomidine: Dexmedetomidine is a centrally acting alpha-2 agonist Desirable

properties include rapid onset and termination of activity, mild to moderate sedation without
significant respiratory depressant action, analgesic effects, and less delirium than the
benzodiazepines. Undesirable properties include a high incidence of bradycardia and
hypotension.
14
Approach to the Patient with Coma Protocol
Version 4.0
Authors
Aarti Sarwal, MD, FNCS, FAAN
Sara Stern-Nezer, MD
Protocol developed by:

Aarti Sarwal,MD, FNCS,FAAN
Sara Stern-Nezer, MD
Approach to the Patient with Coma Algorithm

Checklist
☐ Evaluate/treat circulation, airway, breathing, and cervical spine
☐ Exclude/treat hypoglycemia or opioid/benzodiazepine overdose
☐ Serum chemistries, arterial blood gas, urine toxicology screen
☐ Emergent cranial CT (CT angio brain if appropriate) to determine if coma etiology is
structural or vascular
Communication
☐ Physician and advanced provider communication
☐ Clinical presentation
☐ Relevant past medical history/surgical history
☐ Findings on neurological examination including details on GCS components and any
abnormality with brainstem reflexes, if found
☐ Relevant laboratory tests including glucose, blood gas, renal and hepatic function
☐ Brain imaging, LP, or EEG results (if available)
☐ Treatments administered so far
☐ Nursing, physician/advance practice provider communication
Sample Sign-off Narrative:

64-year-old male patient was found unresponsive at home with agonal respirations. He was
intubated on scene without sedatives, paralytics. Received no medications or infusions
hypertensive in 190 s SBP with no spontaneous respirations on ventilator on controlled
mechanical ventilation at 100% FiO2 with tidal volume of 350 ml and PEEP 8 saturating 95%,
PaCO2 on blood gas was 38 mmHg; 5.06 kPa (goal PCO2 35–40 mmHg; 4.6–5.3 kPa),
absent brainstem reflexes or motor response to pain but pin point pupils. GCS 3. Toxicology
screen showed cocaine. Neurological consults or neuroimaging CT angio are not available
here; hence being transferred.
3
Unconscious Patient
Eyes closed, unresponsive
A patient who has eyes closed and is unresponsive is considered comatose.
Determine unresponsiveness:
• Observation: eyes closed, immobility, lack of facial expression, obliviousness to
environmental stimuli
Examiner evaluates response to graded stimulus:

• Verbal stimulus - Ask "Are you OK?" or "What is your name?" Other auditory
stimulus may be a loud handclap.
• Tactile stimulus to body parts with large cortical representation - face and hands
• Noxious stimulus - should be intense but not cause tissue injury. Recommended
maneuvers include sternal rub, nail-bed pressure, pressure on supraorbital ridge or
on posterior aspect of mandibular ramus.
4
Assess ABCs and C-Spine
The unconscious patient’s ABCs should be quickly assessed and concurrently treated (see
ENLS protocol Airway, Ventilation, and Sedation). Verifying patency of the airway is an
overriding initial priority to ensure adequate oxygenation and ventilation. The patient’s cervical
spine should be immobilized if the possibility of injury cannot be ruled out.
• Airway, breathing and circulation are assessed and concurrently treated as detailed
in ENLS protocol Airway, Ventilation and Sedation
• Rapid survey of head and neck, chest, abdomen, and extremities. Cervical spine is
immobilized if there is any likelihood of traumatic instability.
• Bedside glucose testing is performed on all unconscious patients. If blood glucose is
< 70 mg/dl administer 20-50 ml of 50% dextrose. Thiamine 100 mg IV should be
given prior to dextrose in patients at risk for nutritional deficiency (e.g., chronic
alcohol users, bariatric surgery patients, patients with malabsorptive states) (see
Table 3)
• If there is suspicion of opioid toxidrome (e.g., history of drug use, coma, apnea or
bradypnea, small pupils), administer naloxone 0.04-0.4 mg IV/IM and repeat as
needed in total dosing up to 4 mg. 1–2 mg per nare into both nares can be given
initially but switch to IV/IM when possible (see Table 3).
5
Neurological Assessment
Focused neuro exam
The emergency neurological assessment of the unconscious patient has four parts: level of
consciousness, brainstem assessment, evaluation of motor responses, and appraisal of
breathing patterns. Many scales are available to aide in emergent neurological assessment of
a comatose patient
See Table 4 for Adult Glasgow Coma Scale

See Table 5 for Pediatric Glasgow Coma Scale
See Tables 6 and 7 for pupillary and respiratory changes in different etiologies of coma
See Figure 2 for FOUR Score
• Level of consciousness: Refer to Glasgow Coma Scale (see Tables 4 and 5) or

FOUR Score (see Figure 2). Assess additional potential signs of arousal including
visual fixation, visual pursuit (tracking), and forced eye closure resisting the
examiner.
• Brainstem (cranial nerve) examination:
o Pupillary size, reactivity, and symmetry (see Table 6 for pupillary changes
reflecting underlying etiology)
o Corneal reflex
o Visual threat response
o Oculocephalic reflex (doll’s eyes - only if no suspicion of cervical instability)
o Gag reflex
o Cough reflex
• Motor function: Spontaneous muscle position/posture, spontaneous movements,
response to verbal command, response to noxious stimulus. Examiner should
distinguish purposeful from reflexive activity. Examples of purposeful activity include
following commands, pushing examiner away, reaching for endotracheal tube,
localizing to noxious stimulus. Examples of reflexive activity include withdrawal,
flexion, or extension to noxious stimulus.
• Breathing pattern: The breathing pattern may have localizing value in comatose
patients with brainstem lesions (see Table 7 for respiratory pattern reflecting
underlying etiology)
o Cheynes stokes-global metabolic encephalopathy, impaired forebrain or
diencephalon
o Central neurogenic hyperventilation: metabolic encephalopathy, high brainstem
tumors (rare)
o Apneusis bilateral pons lesion
o Cluster breathing or ataxic breathing - pontmoedullary junction lesion
o Apnea – lesions affecting ventrolateral medulla bilaterally
6
Assess for Readily Reversible Conditions
Prehospital and initial hospital evaluation should focus on assessing and treating readily
reversible conditions like airway compromise, hypotension, hypoglycemia, opioid overdose.
7
STAT CTH
Consider CTA
Head CT will help assess for possibility of acute intracranial process. See Table 1 for
neurological causes of coma that can be discerned with imaging. Use caution in ruling out
ischemic stroke and brainstem pathology as head CT may be negative early on.
Non-contrast cranial CT should be obtained emergently in unconscious patients with a

presumed structural cause of coma and in patients with an unclear cause of coma after initial
assessment of ABCs and cervical spine stabilization.
If an acute ischemic stroke is suspected, cranial CT angiography and CT perfusion can provide
valuable information on vascular patency and regional perfusion. (see ENLS protocol Acute
Ischemic Stroke). Basilar artery thrombosis is a consideration in sudden onset coma and CT
angiography will be diagnostic. If CT alone is done, look at the basilar artery and see if it is
abnormally hyperdense - this may suggest basilar artery thrombosis. A rapid sequence MRI
may be obtained if there is a presumption of hyperacute ischemic stroke or when the cause of
coma is not explained by other tests.
When a CNS infection is being considered, cranial CT with and without contrast should be
obtained to evaluate for abscess, extra-axial fluid collections, hydrocephalus, hemorrhagic
transformation, and vasculitic infarcts.
8
Focused History/PMH
Patient history is obtained concurrently with resuscitative measures. Historical information
elicited from witnesses, friends, family, co-workers, or EMS personnel may suggest the cause
of coma. EMS personnel may have valuable details about the circumstances in which the
patient was found. Medical and surgical history, medications, alcohol and illicit drug use, and
environmental exposures or evidence of trauma should be systematically queried.
The time course of the alteration in consciousness may be helpful in suggesting etiology. An
abrupt onset suggests a stroke, seizure, or a cardiac event with impaired cerebral perfusion. A
more gradual onset of coma suggests a metabolic or possibly infectious process.
9
STAT Labs
Unless a readily reversible cause of unresponsiveness has been discovered and corrected,
additional laboratory work (serum chemistries, CBC,coags, EtOH level, blood gas, urine
toxicology, cultures) is obtained emergently. Point of care (POC) testing should be utilized
where available.
• Serum chemistries including Na, K, creatinine, BUN, and transaminases
• Hematological panel including hemoglobin/hematocrit, platelets, and white blood cell
count; coagulation studies
• Arterial blood gas
• Toxicology: Blood alcohol level; urine toxicology screen for opioids,
benzodiazepines, illicit drugs. (Note: Some toxins that cause unconsciousness are
not detectable in common toxicology screens); acetaminophen
• Microbiology: Urinalysis; urine culture; blood cultures
10
Causes of Coma
Three possibilities
Information accrued so far is used to establish a preliminary impression of either a structural

cause, a nonstructural cause, or an unclear cause. Structural and nonstructural causes of
coma may coexist. Caution must be exercised in patients with non-focal exam and
noncontributory CT head as brainstem stroke or nonconvulsive seizures can present without
focal or structural abnormalities apparent initially. Orofacial dyskinesias and posturing may be
seen in brainstem stroke and may be mistaken for seizures. Please see Tables 8 and 9 for
neurological and non-neurological causes of coma.
11
Unclear Etiology
In many patients, the etiology of coma cannot be easily identified after initial assessment or
emergent non-contrast cranial CT. Advanced imaging like CT angiogram, perfusion imaging or
rapid sequence MRI or contrast imaging should be considered if suspicion of ischemic stroke
or occult pathology exists based on risk factors. If diagnostic uncertainty persists, a lumbar
puncture may be indicated for suspicion of CNS infection, neuroinflammatory and autoimmune
disorders, and suspected central nervous system involvement of hematological or solid organ
cancers. Additionally, when there is clinical suspicion of an aneurysmal subarachnoid
hemorrhage, a LP should be obtained even if the non-contrast CT is negative.
12
Structural
(Focal Exam)
Structural causes of coma include Traumatic Brain Injury, Acute Ischemic Stroke, Intracerebral
Hemorrhage, Meningitis and Encephalitis, and brain tumor and other mass lesions.
Management should be initiated in consultation with Neurology and/or Neurosurgery.
Asymmetric or focal findings on physical examination suggest a localized brain lesion or

disturbance. A structural etiology is suggested by:
• History: trauma, acute onset of symptoms, immunodeficiency, malignancy
• Physical examination: asymmetric cranial nerve findings, asymmetric motor
responses (e.g., hemiparesis)
• Absence of an obvious toxic-metabolic etiology
Unless proven otherwise, coma is presumed to be structural in origin and should be

immediately assessed with a non-contrast cranial CT since emergent neurosurgical
management may be needed.
Patients with a new onset of seizures, a change in seizure pattern, or status epilepticus should
be evaluated for a possible structural focus. See ENLS protocol Status Epilepticus.
13
Nonstructural
Caution must be exercised in patients with non-focal exam and noncontributory CT head as
brainstem stroke or nonconvulsive seizures can present this way.
A nonstructural cause of coma is suggested by:

• Progressive, gradual onset of symptoms
• History of medication, alcohol, or illicit drug use, or environmental toxic exposure
• Non-focal neurological exam with symmetric cranial nerve and motor findings
Table 9 highlights some important, non-neurological causes of coma.
14
Metabolic Coma
Global or metabolic causes
Common nonstructural causes of coma include anoxic-ischemic encephalopathy, seizures,

metabolic alterations, endocrinopathies, systemic infections, CNS infections, medication
overdose, alcohol and illicit drug use, and exposure to nonpharmacologic neurotoxic
compounds (Table 9).
Treatment is guided by the underlying etiology. Where appropriate, specific

antagonists/antidotes should be administered. For example:
• Opioid overdose: naloxone (Table 3)
• Acetaminophen overdose: N-acetylcysteine (Table 3)
• In some cases, a primary metabolic encephalopathy may evolve toward a structural
process, such as acute liver failure leading to cerebral edema and herniation.
• Seizures and status epilepticus commonly are not associated with any detectable
lesion on cranial CT. However, in patients with new onset seizures or a change in
seizure pattern, a structural cause must be excluded with cranial CT or MRI. CNS
infections (e.g., bacterial meningitis) may have no structural correlate on non-
contrast CT or MRI; however, this study should be obtained with and without
contrast to exclude brain abscess. Remember to initiate antibiotics and
dexamethasone prior to the head CT if you suspect bacterial meningitis.
15
Persisting Uncertainty
Next steps
Depending on the history and presentation, advanced imaging like CT angiogram, perfusion
imaging, rapid sequence MRI must be considered if initial CT head is contributory. Stat EEG
may be considered to assess for non-convulsive seizures.
When diagnostic uncertainty persists despite initial assessment, additional test measures
include:
• Non-contrast head CT is obtained in all comatose patients with an undiagnosed
etiology if not done already.
• Consider basilar artery thrombosis (look for a hyperdense basilar artery sign on non-
contrast head CT); CT-Angiography (CTA) or MR-Angiography (MRA) is definitive.
• EEG to evaluate for non-convulsive seizures or status epilepticus, burst
suppression, or patterns consistent with metabolic encephalopathy. Be aware of
dyskinesias seen in brainstem stroke that may mimic seizures
• Lumbar puncture (LP) is obtained if there is suspicion of CNS infection,
inflammation, infiltration with lymphoma or malignant cells, or to substantiate a
suspicion of aneurysmal subarachnoid hemorrhage in patients with negative CT
findings. A space occupying lesions should be ruled out with non-contrast head CT
prior to performing the LP.
• MRI is obtained when the cause of coma is not explained by other tests or if there is
a presumption of hyperacute ischemic stroke.
• Consultation with a specialist.
16
Intracerebral Hemorrhage Protocol
Version 4.0
Authors
Arthur M. Lam, MD, FRCPC, FNCS
Vineeta Singh, MD
A.M. Iqbal O'Meara, MD
Last updated: March 2020

Intracerebral Hemorrhage Algorithm

Checklist
☐ Complete blood count with platelet count, PT, PTT, INR
☐ CT head results: hematoma size, location, presence of intraventricular hemorrhage
☐ Glasgow Coma Scale (GCS) score
☐ Calculate ICH score
☐ Interventions:
☐ Coagulopathy reversal (goal INR ≤ 1.4)
☐ Blood pressure lowering (goal systolic 140–180 mmHg)
☐ Surgical hematoma evacuation (if indicated)
☐ Airway/ventilation management
Communication
Prehospital to ED (before diagnosis of ICH)
□ Airway status—patent airway/supraglottic device/endotracheal tube
□ Breathing—respiratory status
□ Blood pressure and pulse
□ Age/gender
□ GCS, pupils
□ Signs and symptoms
□ Last known normal
□ Brief relevant medical history—previous stroke, blood thinners, bleeding
□ Current medications
Sample EMS call
“This is Medic 1 with a stroke alert—85-year-old male, acute right hemiparesis, on
aspirin 81 mg. Last known normal at 1300. Vital signs stable. ETA30 min.”
Hand-off after ICH diagnosis has been made

□ Age
□ GCS, pupil exam
□ Hematoma volume and location
□ Other CT findings (intraventricular hemorrhage, hydrocephalus, spot sign)
□ ICH score
□ Airway status
□ Blood pressure, target, and treatment initiated
□ Coagulation parameters (INR, PT, PTT, platelet count, WBC, Hgb) and reversal
treatment if any
□ Medications given
3
□ Plan for surgery if any
Sample Sign-Off Narrative
“I am signing out a 62-year-old man with known hypertension and atrial fibrillation who
is presumed to be on warfarin.”
“He was found at home this morning at 9 AM by his wife who last saw him normal at 7
AM. He was talking to EMS and had left-sided weakness, GCS in
the field was 13, and BP was 170/100.”
“On arrival to the ED here, he was the same, so we drew labs and sent him for a head
CT.”
“CT completed at 10 AM showed a 20 ml right thalamic ICH with mild IVH, but no
hydrocephalus. There is about 4 mm of right-to-left midline shift.
CTA/CTP showed no AVM or aneurysm, but there is a positive spot sign.”
“When he returned to the ED, he was sleepier, with a GCS of 9, and his left-sided
weakness was worse. So he has an ICH score of 2. His labs came back
with an INR of 1.9.”
“We intubated him using rocuronium and etomidate. PCC infusion of 2250 IU (estimated
weight 90 kg; dose of 25 IU/kg) is going in now. He also had
10 mg of IV vitamin K.”
“Neurosurgery has been called, and they are on their way to see him. He is in ED
Resuscitation Room 1, intubated and sedated now on propofol at 60
mcg/kg/min and fentanyl 50 mcg/hr. His BP is 140/85 with no other treatment.”
4
Intracerebral Hemorrhage (ICH)
Initial Diagnosis
Intracerebral Hemorrhage (ICH) typically produces a sudden, new headache followed by

progressive neurological signs. The onset is usually sudden and the neurological symptoms
progress over a few hours likely due to continued intracerebral bleeding. It is not possible to
be certain whether the stroke is due to hemorrhage or ischemia based on signs and symptoms
alone, so some form of emergent brain imaging is necessary.
Intervention for ICH is classified as "primary" meaning what can be done to impact the patient
right now, and "secondary" once these primary interventions are addressed. One should
consider the secondary interventions of blood pressure control, declining neurological exam
requiring airway protection, concurrently.
5
Adequate Airway
Is the patient's airway stable?
ICH may continue to expand and the patient's mental status, and airway may become
compromised. Continued airway assessment is critical, especially in posterior fossa
hemorrhages. Therefore, frequent neuro checks are important in this early phase of ICH to
identify and intervene in a patient who is declining. In general, if an ICH patient is comatose,
rapid sequence intubation (RSI) should be undertake with a goal of normoventilation.
See ENLS protocol Airway, Ventilation and Sedation for discussion on how to intubate.
6
Non-Contrast CT
It is not possible to be certain whether the stroke is due to hemorrhage or ischemia based on
signs and symptoms alone, so some form of emergent brain imaging is necessary. Non-
contrast computed tomography (CT) is the most commonly used modality given that it can be
done quickly, can be used for critically ill patients, and has a very high sensitivity and
specificity for acute parenchymal hemorrhage.
Other findings – Contrast CT, Spot Sign
If IV contrast was administered during the CT scan, extravasation of contrast within the
hematoma may suggest active bleeding. This is called the spot sign as shown in the figure:
7
Brief Medical and Medication History
As with all strokes, it is important to obtain a brief history on the onset of symptoms and when
the patient was last seen normal. Prehospital providers should attempt to get a medical history
and list of medications prescribed for the patient with specific attention to antiplatelets,
anticoagulants, and antihypertensive medications.
8
BP Control
Should BP be lowered?
Target SBP between 140 and 180 mmHg with the specific threshold determined based on
patient comorbidities and level of chronic hypertension; consider using IV nicardipine, IV
clevidipine with or without IV labetalol.
Keep SBP between 140-180 mm Hg with the specific threshold determined based on patient
comorbidities and level of chronic hypertension; consider immediate treatment with IV labetalol
and using IV nicardipine or IV clevidipine infusion to maintain control.
See ENLS Pharmacotherapy module for details on IV antihypertensive dosing.
9
Hemostasis
Is there an underlying coagulopathy?
If yes, consider presence of oral or parenteral anticoagulants, antiplatelet agents, liver failure
and DIC.
Anticoagulants and DIC, INR > 1.4
See the ENLS reference Pharmacotherapy module for a detailed listing of medications and
dosing for reversal of anticoagulant drugs.
Rapid vitamin K antagonist reversal is recommended with purified factor concentrates or FFP if
patient has taken warfarin or other vitamin K antagonists concurrent with vitamin K 10 mg IV
administered by slow IV push. 4-factor prothrombin complex concentrates (PCC) are superior
to FFP. Weight based dosing for PCC (or FFP only if PCC is not available) with the dose
adjusted based on INR is recommended.
For patients with ICH and having taken dabigatran, idarucizumab may be used to reverse the
anticoagulant effects of dabigatran. The recommended dose of idarucizumab is 5 g, provided
as two separate vials each containing 2.5 g/50 mL idarucizumab. Activated charcoal (50 gm)
should also be given if ICH occurs within 2 hours of most recent dabigatran dose. If
idarucizumab is not available, consider activated PCC FEIBA or 4 factor PCC; these
approaches have not been formally tested and do not fully reverse dabigatran coagulopathy.
Andexanet alpha is now approved as a specific reversal agent for direct Xa inhibitors. For
dosing, depending on the agent that the patient is on, please refer to ENLS Pharmacotherapy
module.
Antiplatelet Agents
If the patient has been taking antiplatelet drugs (aspirin, clopidogrel, prasugrel, etc.), it is
reasonable to transfuse with platelets if they are undergoing a neurosurgical procedure and
consider administering single dose of DDAVP 0.4 mcg/kg IV.
Heparin + Recent Heparin Administration
Administer protamine sulfate IV 1 mg per 100 U heparin received in last 2 hours; maximum
dose 50 mg IV. Protamine sulfate in the same dose can be used in an attempt to reverse the
effect of low molecular weight heparin that was given within the prior 8 hours, but this reversal
may be incomplete.
See ENLS Pharmacotherapy module for details on IV anticoagulant reversal dosing.
10
Consider Surgery
Is the patient a surgical candidate?
Cerebellar ICH should be considered for surgery urgently depending on size. Typically,
surgery is considered for hematomas in excess of 3 cm in any dimension or with compression
of the brain stem or hydrocephalus and neurosurgery should be consulted urgently.
Consider surgery for lobar ICH with mass effect in severely affected but salvageable patients
and as a life-saving measure in patients who are herniating. Decompressive hemicraniectomy
might be considered a life saving measure in deteriorating patients.
11
ICP Management
Current guidelines for ICP monitoring in ICH follow the approach in severe traumatic brain
injury, with ICP monitoring recommended in patients with GCS ≤ 8, large hematomas with
mass effect suggestive of elevated ICP, or hydrocephalus. As a goal, an ICP < 22 mmHg
should be maintained, with a minimal CPP of 60 mmHg, adjusted based on an individual
patient’s cerebral autoregulation status. A CPP between 60 and 70 mmHg is reasonable,
based on current Brain Trauma Foundation Guidelines on CPP threshold. (Note this
recommendation is based on patients with severe traumatic brain injury.) Ventricular catheters
are beneficial in their ability to both measure ICP and drain cerebrospinal fluid (CSF);
therefore, they should be used in patients with hydrocephalus. In contrast, intraparenchymal
fiberoptic monitors have a lower risk of hemorrhage and infection, but cannot be used to drain
CSF. Correction of coagulopathy prior to ICP monitor insertion is desirable to minimize the risk
of hemorrhage. An INR ≤ 1.5 is recommended prior to EVD insertion.
See ENLS Intracranial Hypertension and Herniation module for management

recommendations.
12
Characterize ICH
Measure the hematoma volume
If the blood is within the brain parenchyma, use the ABC/2 method.
ABC/2 method for estimating ICH hematoma volume. Right basal ganglia intracerebral
hemorrhage. The axial CT image with the largest cross sectional area of hemorrhage is
selected. In this example, the largest diameter A is 6 cm, the largest diameter perpendicular to
A on the same image B is 3 cm, and hemorrhage is seen on 6 slices of 0.5 cm (5 mm)
thickness for a C of 3 cm (not shown). Thus, the hematoma volume is (6 X 3 X 3)/2 = 27 cc.
Note that for C, if the hematoma area on a slice is approximately 25-75 % of the hematoma
area on the reference slice used to determine A, then this slice is considered half a
hemorrhage slice, and if the area is <25 % of the reference slice, the slice is not considered a
hemorrhage slice.
13
Calculate the ICH score
The ICH score can be calculated as follows:
Component Criteria Points

GCS 3-4 2
5-12 1
13-15 0
ICH Volume  30 ml 1
< 30 ml 0
Intraventricular hemorrhage Yes 1
No 0
Infratentorial origin Yes 1
No 0
Age  80 years 1
< 80 years 0
Total 0-6
The ICH score is a method to determine severity of illness and as a communication tool among
providers rather than as a tool to precisely prognosticate outcome. Although it is correlated
with mortality, one should not use any particular score to limit care.
Location of ICH
ICH tends to occur in characteristic locations, with hypertensive ICH most frequently located in
the basal ganglia, thalamus, pons (brainstem), cerebellum. ICH due to cerebral amyloid
angiopathy or AVM tends to have a lobar location. May occur in more than one site. The origin
of the hematoma is usually evident from the initial CT scan, and its location influences
outcome and treatment.
14
Typical locations for ICH. ICH due to chronic hypertension is usually due to rupture of small
penetrating arterioles and typically occurs in the basal ganglia (A), thalamus (B), cerebellum
(D), and pons (E). ICH from cerebral amyloid angiopathy and sympathomimetic drugs of abuse
such as cocaine or methamphetamine often occurs in lobar regions such as the temporal lobe
(C). Supratentorial ICH would be considered as basal ganglia, thalamic, or lobar (A-C),
whereas ICH originating in the cerebellum or pons would be considered infratentorial (D-E). A,
B, and E also demonstrate IVH.
15
Transfer
NCCU, surgery, or another institution
NCCU admission is preferable. If a NCCU bed is not available, then general ICU admission is
preferred. The key is to have frequent neuro checks in patients who may suffer a decline in
neurological and/or airway status so interventions can occur quickly. If the patient is not
ventilated and not on IV antihypertensive agents, then a step-down unit is an alternative as
long as frequent neuro checks can be obtained.
If the patient is a surgical candidate, then direct transfer to the OR may be an option.
If ICU/NCCU services are not available or surgery is not available, consider emergent transfer
to an institution with these services. Critical care transportation may be necessary depending
on airway status, hemorrhage location and size, and judgment about the risk of neurological
worsening in transport.
16
Intracranial Hypertension and
Herniation Protocol
Version 4.0
Authors
Jonathan J. Ratcliff, MD, MPH
Christopher Morrison, PharmD, BCCCP, FNCS
Christopher M. Ruzas, MD
Last updated: March 2020

Intracranial Hypertension and Herniation Algorithm
Communication
Intracranial Hypertension and Herniation Protocol
Communication
□ Age
□ Injury mechanism (e.g., intracerebral hemorrhage, trauma, acute ischemic stroke, etc.)
□ Relevant known medical history
□ Comorbid or complicating conditions
□ Suspected etiology for elevated ICP/Herniation (e.g., diffuse edema after trauma)
□ Clinical neurological examination (worst, best, and current exam seen during your care)
□ Steps taken to manage ICP and patient’s response to intervention
□ Anticipated next steps (e.g., continue 23.4% for sodium goal > 145 mEq/L with q4 h checks)
•Does the patient have an EVD or other ICP monitor?
•What is the patient’s vascular access?
Sample sign-off narrative:
56-year-old male who is status post motor vehicle collision in which he was an unrestrained
driver.
The patient’s primary survey was significant for failure to protect his airway, due to his mental
status, requiring endotracheal intubation—which was performed without complication.
Breathing and circulation were intact; his GCS (E2V3M3) was 8 before being intubated with a
left pupil 7 mm and nonreactive and 4 mm reactive pupil on the right.
He was given 150 ml of 3% HTS for his large, nonreactive, pupil and was hyperventilated to an
EtCO2 of 30. His pupil improved after these interventions.
His CT head revealed a large subdural hematoma with 6 mm of midline shift.
The patient is going directly to the operating room for hematoma evacuation.
He has no ICP monitor at this time and has 3–16 g peripheral IVs.
3
Intracranial Hypertension and/or Herniation

ICP > 20 mmHg or Clinical Signs
Sustained intracranial hypertension and acute brain herniation are “brain codes,” signifying
catastrophic neurological events that require immediate recognition and treatment to prevent
irreversible injury and death. As in cardiac arrest, a brain code mandates the organized
implementation of a stepwise management algorithm. The goal of this Emergency Neurological
Life Support protocol is to detail an evidence-based, standardized approach to the evaluation
and management of patients with intracranial hypertension and/or herniation.
Although frequently linked, elevations of ICP and brain herniation can occur independently.
• Intracranial hypertension is defined as a sustained (> 5 min) elevation of ICP to > 22
mmHg.
• Detection requires invasive monitoring, but certain clinical and physiological signs may
suggest elevated ICP prior to instrumentation.
• Herniation syndromes result from intracranial compartmental pressure gradients leading to
parenchymal tissue shifts that compress or displace the brainstem, cranial nerves, or
cerebral vasculature.
• Ischemia or infarction during such vascular compression may cause edema and further
aggravate a deterioration in compliance.
Diagnosis
• Clinically, symptoms of increased ICP include headache, nausea and vomiting, pupillary
changes, and/or altered mental status.
• Patients with increased ICP may demonstrate physical signs of hypertension, bradycardia,
and irregular respirations or apnea (Cushing’s triad), although the concurrence of all three
signs is an uncommon and often late finding.
• Common sites for herniation are the cingulum of the medial frontal lobe (subfalcine
herniation), medial temporal lobe (uncal herniation), and inferior cerebellum (tonsillar
herniation).
• The cardinal signs of transtentorial (uncal) herniation are an acute change in
consciousness associated with ipsilateral pupillary dilation and contralateral hemiparesis,
resulting, respectively, from compression or displacement of ascending arousal pathways,
oculomotor nerve(III), and corticospinal tract.
4
Tier Zero
Standard issues to prevent herniation
It is important to stress that any patient who is at risk for elevated ICP should have the Tier
Zero interventions in place.
• Assess ABCs – assess airway patency, ventilation, and adequate circulation
• Minimize noxious stimuli such as tracheal suctioning that may elevate ICP
• Analgesia/sedation
• Target normothermia. If hyperthermia is present, measures should be taken using targeted
temperature management (TTM) to normalize body temperature to 36–37.4 °C
• The head of the bed should be elevated to > 30°, and the head is kept midline to facilitate
cerebral venous drainage
• Neck midline
• Only iso- or hyperosmotic fluids should be used as intravenous (IV) solutions
• Avoid and correct hyponatremia (serum Na < 135 mEq/L)
• High-dose corticosteroid therapy is initiated for vasogenic edema resulting from brain
tumors, abscesses, or non-infectious neuroinflammatory conditions but should otherwise be
avoided
• If the brain has not yet been imaged, a non-contrast head CT scan should be performed
when the patient can be positioned safely for diagnostic imaging
5
Tier One
Hyperosmolar therapy, hyperventilation, CSF drainage, surgery
Hyperosmolar therapy
• Mannitol or hypertonic saline (HTS) have shown equivalent efficacy in lowering of ICP –
see ENLS Pharmacotherapy module.
• To be effective, intact blood brain barrier and osmotic/sodium gradient between brain
and serum are required to promote the egress of water from the brain.
• Mannitol is administered as 0.5–1 g/kg IV bolus through a peripheral IV line over 5–15
min and may be repeated every 4–6 h. Repeat dosing of mannitol can be determined
based on the osmolar gap which is derived as the difference between measured and
calculated osmolality.
• No therapeutic benefit is appreciable with osmolar gap > 20 mOsm/kg.
• HTS is available in concentrations from 2 to 23.4% and can be administered as a bolus
alone or in addition to mannitol.
• HTS concentrations boluses ≥ 7.5% should be given via a central venous catheter;
when using concentrations lower than this, peripheral lines may be used, but the
infusion should be in a large vessel, and the IV site should be carefully monitored for
infiltration.
• When infusing HTS, serum sodium concentration levels should be checked every 4–6 h,
and serum sodium concentrations should be kept < 160 mEq/L.
• Administration of HTS through intraosseous (IO) access should be done with caution
and only with concentrations of 7.5% or less due to uncertain risk of myonecrosis.
Temporary hyperventilation to a PaCO2 of 30–35 mmHg

• A brief course (< 2 h) of hyperventilation to a PaCO2 of 30–35 mmHg may be
considered, while definitive treatment is provided
CSF drainage
• Acute obstructive hydrocephalus, as determined by neuroimaging, should be
emergently managed with an external ventricular drainage (EVD) system. If an EVD
system is already in place, drain 5–10 ml of CSF for acute rises in ICP [22].
Consider surgical decompression

• If ICP is not controlled, and/or clinical signs of herniation do not resolve with Tier One
interventions, decompressive surgical options (e.g., evacuation of hemorrhagic
contusion) should be considered
If surgery is not appropriate or not undertaken, Tier Two interventions should be implemented.
If ICP is controlled with Tier One interventions, consider repeating the head CT scan to rule out
new processes.
6
Tier Two
Hypertonic saline and sedation
If Tier One interventions have failed to control ICP, Tier Two should be engaged.
Hyperosmolar therapy for higher Na goals

If hyperosmolar therapy with HTS has been administered, serum sodium goals may be
increased if they are not yet at a maximal concentration.
• In practice, serum sodium concentration > 160 mEq/L is unlikely to provide significant
additional benefit.
• Once the ICP has stabilized, sodium concentration should be maintained at the current
concentration until the brain edema has improved. This is often achieved with
intermittent boluses of 3% NaCl during which serum sodium levels are monitored every
6 h.
• It is controversial whether continuous infusion of 3% NaCl is beneficial for ICP control.
Optimize sedation and analgesia

Sedation may be increased to aid in ICP management.
• Propofol has been shown to reduce cerebral metabolic demand (CMRO2) and cerebral
blood volume (CBV) and, consequently, ICP.
• Administer propofol as a bolus of 1–2 mg/kg. May be continued as an infusion (titrate to
maximum 200 μg/kg/min) in ventilated patients.
• Propofol, especially when given as a bolus dose, is associated with circulatory
depression, which should be corrected with IV fluids and/or vasopressors to maintain
CPP goals.
• A small subset of patients receiving propofol may develop a propofol infusion syndrome
characterized by metabolic acidosis, cardiac dysfunction, rhabdomyolysis, and
hypertriglyceridemia, often with a fatal outcome.
• Propofol infusion syndrome is more likely to develop at doses greater than > 70
mcg/kg/min administered for > 48 h. If propofol is infused at these extreme doses (200
μg/kg/min), it should only be done temporarily, while other corrective measures are
executed.
Rescue decompressive surgery should be considered as a life-saving intervention.
7
Tier Three
No longer a surgical candidate
Tier Three measures represent the most aggressive level of management and also carry the
highest risk of adverse effects. Rigorous randomized prospective studies are lacking, and
recommendations are driven by consensus.
Sedation titrated to ICP goal or burst suppression on cEEG

• This tier includes administration of pentobarbital (bolus 5–15 mg/kg over 30 min—2 h,
then maintenance infusion of 1–4 mg/kg/h) titrated to ICP goal or burst suppression on
continuous electroencephalogram (EEG).
• Some patients may not tolerate pentobarbital bolus at these doses because of
cardiovascular complications, such as hypotension.
• Often arterial vasopressors are necessary for hemodynamic support.
• EEG should be continuously monitored, and pentobarbital titrated either to ICP or to
EEG burst suppression of 5–20 s or at least 50%.
• The pentobarbital infusion is continued for 24–96 h, while the processes driving ICP are
treated.
• Pentobarbital is associated with respiratory depression, cardiovascular instability,
immune suppression, and paralytic ileus. During treatment, the neurological
examination is limited by sedation. High-dose pentobarbital can mimic signs of brain
death including unreactive pupils even by pupillometry and caution is to be exercised in
prognostication, as pentobarbital plasma clearance may take days after discontinuation
of infusion; however, redistribution from the CNS occurs more rapidly.
Hyperventilation to achieve mild to moderate hypocapnia (PaCO2 25-34 mmHg)

• Hyperventilation to achieve mild-to-moderate hypocapnia (PaCO2 25–34 mmHg) may
be considered in selected patients who have failed other management in the acute
period.
• Prolonged hyperventilation, for more than 6 h, is unlikely to be beneficial and may cause
or exacerbate ischemic injury due to hypocapnia-associated cerebral vasoconstriction.
Hence, hyperventilation should ideally be accomplished in conjunction with a cerebral
oxygen monitoring (e.g., jugular venous oximetry, brain tissue oxygen monitoring) to
detect cerebral ischemia.
Moderate hypothermia (target core temperature 32–34°C)

• TTM for mild hypothermia (target core temperature 32–34 °C) may be associated with a
reduction in ICP but has not been shown to result in improved outcomes
• TTM for mild hypothermia may be induced with external surface cooling devices, IV
infusion of cooled fluids, or intravascular or esophageal cooling devices
• Hypothermia may be associated with shivering, cardiac arrhythmias, sepsis, and
electrolyte disturbances, and protocols for induction, maintenance, and rewarming
should be used to prevent or treat these complications.
8
Meningitis and Encephalitis Protocol
Version 4.0
Authors
Katharina M. Busl, MD, MS
Ricardo A. Hernandez, MD
William J. Meurer, MD, MS
Sarah Peacock, DNP, APRN, ACNP-BC
Sandra D.W. Buttram, MD

Meningitis and Encephalitis Algorithm
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Checklist
☐ Vital signs, history, examination

☐ Contact and droplet precautions (until pathogen classified)
☐ IV access
☐ Labs: CBC, PT/PTT, chemistries, glucose, blood cultures, lactate
☐ IV fluids, treat shock
☐ Immediate administration of dexamethasone followed by appropriate antibiotics for
presumptive bacterial meningitis
☐ Consider acyclovir (if herpes simplex virus is a concern)
☐ Head CT, if patient neurological exam abnormal
☐ Lumbar puncture (LP), if CT results available
☐ If meningococcus remember exposure prophylaxis for contacts
Communication
☐ Presenting signs, symptoms, vital signs on admission and relevant past medical history
☐ Relevant laboratory results including white blood cell count, bicarbonate level, lactate level,
and renal function
☐ Head CT and results if obtained
☐ IV fluid administered, input/output
☐ Antibiotics administered and time started; dexamethasone if given
☐ Results of LP, including opening pressure
☐ Current vital signs, pretransfer physical and neurological exam
☐ Ongoing concerns, active issues, outstanding studies/tests
☐ Infectious precautions applied/required
3
Suspicion of Meningitis or Encephalitis
Fever, headache, altered mental status, stiff neck
Patients that have a hyper-acute (hours) and acute (hours to days) onset of headache and
altered mental status should be considered to have meningitis or encephalitis. Additional signs
of meningismus, fever, new rash, focal neurological findings or new onset seizure significantly
increase the suspicion of CNS infection.
Infants often have non-specific manifestations of CNS infection such as fever, hypothermia,
lethargy, irritability, respiratory distress, poor feeding, vomiting, or seizures. In older children,
clinical manifestations include fever, headache, photophobia, nausea, vomiting, and decreased
mental status.
As with all acute medical and neurological events, the basics of ABC (airway, breathing and
circulation) should be evaluated early in the Emergency Department course. Patients with
altered mental status are at high risk for airway compromise and should be monitored closely
for needing intubation. Likewise, patients with bacterial meningitis are at risk for lung or
bloodstream infections with the same pathogen, and as such, vital signs and hemodynamics
need to be monitored closely to diagnose sepsis.
Meningitis is defined as inflammation of the meninges (and will have an abnormal LP) while
encephalitis is defined as inflammation of the brain (and the LP is usually normal). If both are
inflamed, the patient has meningoencephalitis. Meningitis causes fever, meningismus (flexion
limitation of neck when fully supine), and pain (head and/or neck) but other than depressing a
patient’s mental status, does not affect any cortical function. Encephalitis on the other hand
typically causes cortical disturbances (seizures, aphasia, hemiparesis, etc.). In pure
encephalitis, the spinal fluid is free of white cells, but protein may be elevated. Once white
cells are found in the spinal fluid, some form of meningitis is also present.
The two conditions that are most important to recognize in the first hour are bacterial
meningitis and herpes encephalitis as these diseases have specific treatments that can
improve patient outcome if administered quickly.
Fever
Measuring oral temperature is adequate. Both fever (temperature > 38°C) or hypothermia
(temperature < 35°C) are compatible with CNS infection. If the patient is euthermic, the pretest
probability of bacterial meningitis or HSV encephalitis is decreased. However, newly
immunocompromised patients, patients with viral meningitis, and even a rare patient with
bacterial meningitis may present euthermic. Depending on other signs and symptoms, it may
be appropriate to stop here and work-up other causes of headache.
Headache
The presence of a new, never experienced headache is a significant symptom that needs
work-up on its own merits. If the headache is sudden in onset (i.e. a thunderclap headache
within seconds) this suggests subarachnoid hemorrhage (SAH). Patients with SAH can have
fever because blood in the meninges causes a chemical meningitis. If the headache is typical
4
of the patient’s usual headache, one should not completely dismiss this symptom’s importance
as meningitis and encephalitis will cause exacerbation of a pre-existing headache disorder.
Lastly, it is quite uncommon to have meningitis without headache or neck pain, but less
uncommon in encephalitis.
Altered Mental Status

CNS infections typically depress the level of consciousness (see the ENLS protocol Coma).
Infants may be lethargic, stop eating, and become irritable. Adults typically become somnolent
then stuporous. Delirium is common with the chief objective sign of inattentiveness (can’t
repeat back serial digits). Sepsis can compound the mental status if significant hypotension is
present. Elderly patients or patients with pre-existing neurological conditions may become
agitated and combative.
Stiff Neck/Meningismus
Meningitis causes reflex contraction of the erector spinae muscles causing limitation in passive
neck flexion (meningismus). Patient may complain of neck stiffness or pain, but many do not,
so this symptom has poor negative predictive value. To test for the sign of meningismus,
place the patient fully supine (completely flatten the bed and remove the pillow), then rotate the
head on neck. You should feel no resistance to rotation if the patient is fully relaxed. Then,
ask the patient to not resist, place you hand under their head, and slowly flex the head on the
neck and see if you can fully flex the neck so that the chin touches the manubrium. If it does,
meningismus is absent. If there is a limitation, it typically occurs at a specific degree of flexion
and beyond. Measure the distance from the chin to the chest with your fingers and report the
degree of flexion limitation as the number of finger breadths you can place in-between. If the
patient resists flexion to all degrees, especially if there is resistance to head rotation,
meningismus may be present but this finding is less specific. Do not test for neck flexion
limitation if the patient is standing or sitting as this produces false negatives; the patient must
be fully supine.
5
Begin Resuscitation, Start Antibiotics
Empirical treatment
If the patient meets SIRS criteria (hypotension, fever), an initial fluid bolus of 30 ml/kg of
crystalloid solution should be immediately infused over 20-30 minutes, and the patient’s vital
signs, mental status, and airway should be reassessed every 5 min during this phase of
treatment. If IV access cannot be obtained within a few minutes of presentation, interosseous
access should be placed. Antibiotics should be given concomitantly with IV fluids, or
immediately after starting IV fluids, and should never be delayed.
Select the appropriate antibiotics/antivirals based on a) the course of the suspected CNS
infection, b) age of the patient, and c) other infectious risk factors
• Children < 2 months are at risk for group B streptococci (GBS), Escherichia coli,
Listeria monocytogenes, Streptococcus pneumonia, Haemophilus influenzae and
Neisseria meningitidis. Use IV ampicillin, gentamycin, and cefotaxime.
• In older infants (2 to 23 months), children, and adolescents, the causes as typically
Streptococcus pneumoniae (which may be penicillin resistant), Neisseria
meningitides, and Haemophilus influenzae. In the younger patients in this group,
GBS may still occur. Administer vancomycin plus either cefotaxime or ceftriaxone.
The empiric antibiotic regimen should be broadened in infants and children with
immune deficiency, recent neurosurgery, penetrating head trauma, or other
anatomic defects
• Young adults with suspected bacterial meningitis are at risk for Haemophilus
influenzae (if not vaccinated), Neisseria meningitidis, and Streptococcus
pneumoniae. As such, they should be started on a 3rd generation cephalosporin
and vancomycin at doses appropriate for CNS penetration.
• Middle-aged adults are at highest risk for Streptococcus pneumoniae. As such, they
should be started on a 3rd generation cephalosporin and vancomycin at doses
appropriate for CNS penetration. Vancomycin can be used alone in patients with a
severe penicillin allergy.
• The elderly and immunosuppressed are at risk for Streptococcus pneumoniae and
Listeria monocytogenes. As such, they should be started on ampicillin, a 3rd
generation cephalosporin and vancomycin at doses appropriate for CNS
penetration. Vancomycin for S. pneumoniae, and trimethaprim-sulfamethoxazole for
Listeria, can be used in patients with a severe penicillin allergy.
• For suspected CNS infections that evolve over days, consider viral encephalitis,
particularly herpes simplex encephalitis. Treatment should begin with acyclovir at
10mg/kg every 8 hours. IV hydration should be sufficient to achieve normovolemia.
This avoids the complication of acyclovir-associated renal failure.
• For suspected CNS infections that evolve over days in an immunosuppressed
patient, consider fungal meningitis. If there is a high index of suspicion for fungal
meningitis, such as prior history of fungal CNS disease or systemic fungal infections,
and rapid disease progression, empiric amphotericin B can be considered.
6
• TB meningitis is another CNS infection to be considered in the early differential
diagnosis, espe-cially if there has been a subacute and more protracted course of
onset of illness: In a patient pre-senting with a symptom duration of more than 5
days, particularly if the patient is immunocom-promised, the diagnosis of TB
meningitis should be considered. Tuberculosis is more preva-lent in high-risk
groups, including the homeless, nursing home residents, ethnic minorities, and
persons infected with HIV. Empiric treatment regimens are largely based on those
for pulmonary TB.
There is evidence supporting the use of dexamethasone in bacterial meningitis, particularly in

CNS infections caused by Streptococcus pneumoniae, an Haemophilus influenzae. In a
Cochrane systematic review and meta-analysis, it was found that corticosteroids overall
reduced the rate of any hearing loss, severe hearing loss, and neurological sequelae.
Subgroup analyses showed that corticosteroids a) prevented hearing loss in children with
bacterial meningitis b) reduced severe hearing loss only in children with meningitis due to H.
influenzae, c) reduced mortality in Streptococcus pneumoniae but not for other bacteria and d)
protected against severe hearing loss and short term sequelae for children in high-income
countries, but not for those in low-income countries. Adjunctive corticosteroids are also
recommended for TB meningitis regardless of disease severity.
Give dexamethasone 10 mg IV, ideally given 10 to 20 minutes before antibiotics, or with the
first dose of antibiotics, until up to 4 hours after the first antibiotic dose. Corticosteroid
administration should not delay the administration of IV antibiotics. Other corticosteroids can
be used in equivalent doses if dexamethasone is not available. Dexamethasone is the
preferred corticosteroid, when these agents are used, due to superior penetration into the
cerebrospinal fluid (CSF) and a longer half-life. There is insufficient data to recommend
starting corticosteroids in neonates.
TARGET AGENT CHILDREN ADULTS

BACTERIAL
Group B Streptococci Ampicillin 0 to 7 days: 100 2 g IV every 4 h
Listeria mg/kg/dose IV every
Gram-negative bacteria 8-12 h
(E. coli)
8 to 28 days: 50-100
mg/kg/dose IV every
6-8 h
> 28 days: 50
mg/kg/dose IV every
6 h (MAX: 12 g/day)
H. influenzae Ceftazidime 0 to 7 days: 50 2 g IV every 8 h
N. meningitidis mg/kg/dose IV every
8-12 h
7
P. aeruginosa > 7 days: 50
S. pneumoniae mg/kg/dose IV every
8h
H. influenzae Cefotaxime 0-7 days: 50 2 g IV every 4-6 h
N. meningitides mg/kg/dose IV every
P. aeruginosa 8-12 h
S. pneumoniae 8-28 days: 50
mg/kg/dose IV every
6-8 h
>28 days: 75
mg/kg/dose IV every
6-8 h
H. influenzae Ceftriaxone Neonatal: 2 g IV every 12h
N. meningitidis < 14 days: 50 mg/kg
S. pneumoniae IV once daily
≥ 14 days: 100 mg/kg
X1, then 80-100
mg/kg/day IV once
daily
Infants/children:
80-100 mg/kg/day
divided every 12-24
hours
(Maximum dose: 4
g/day)
S. aureus Vancomycin 15 mg/kg/dose IV 15-20 mg/kg/dose IV
S. pneumoniae every 6 h every 8 -12 h
Enterococcus species Gentamicin Neonates: 4-5 5 mg/kg/day IV in divided
Listeria mg/kg/dose IV every doses every 8 h
monocytogenes 24-36 h
S. agalactiae
P. aeruginosa Infants/children: 2.5
mg/kg/dose IV every
8h
H. influenzae Meropenem 40 mg/kg/dose IV 2 g IV every 8 h
N. meningitidis every 8 h
S. pneumoniae
Alternative in penicillin Aztreonam 30 mg/kg/dose IV 2 g IV every 6-8 h
allergy every 6-8 h (MAX: 8
- component of empiric g/day)
therapy
- H. influenzae
Enterobacteriaceae
P. aeruginosa
8

VIRAL
Herpes simplex virus Acyclovir Birth to 12 years old: 10 mg/kg/dose IV every 8
20 mg/kg/dose IV h
every 8 h
12 years or older: 10
mg/kg/dose IV every
8h
Varicella-Zoster virus Acyclovir Birth to 12 years old: 10 mg/kg/dose IV every 8
20 mg/kg/dose IV h
every 8 h
12 years or older: 10
mg/kg/dose IV every
8h
Or
Ganciclovir 5 mg/kg/dose every 5 mg/kg/dose IV every 12
12 h h
Cytomegalovirus (in Ganciclovir 5 mg/kg/dose every 5 mg/kg/dose every 12 h
HIV-infected) 12 h plus foscarnet plus foscarnet until
until symptoms symptoms improve*
improve
*off-label
9

FUNGAL
Candida species Amphotericin B 5 mg/kg/dose IV daily 5 mg/kg/dose IV daily
Aspergillus species lipid complex (may premedicate (may premedicate with
Mucorales with acetaminophen + acetaminophen +
Mycoses antihistamine to antihistamine to prevent
Molds prevent infusion infusion reactions)
Leishmania species reactions)
Cryptococcus Liposomal 3-5 mg/kg/day IV 3-6 mg/kg/day IV daily
Empiric in febrile amphotericin B daily (may premedicate with
neutropenic patients (may premedicate acetaminophen +
with acetaminophen + diphenhydramine to
diphenhydramine to prevent infusion
prevent infusion reactions)
reactions)
10

MYCOBACTERIAL (initial intensive phase)
Empiric for strong Ethambutol Weight-based: <15 years and ≤40 kg: 15
suspicion of to 25 mg/kg/day
tuberculous meningitis: 40- 55 kg: 800 mg PO 40-55 kg: 800 mg PO
combination regimen (4 daily daily
drugs) 56-75 kg: 1200 mg 56-75 kg: 1200 mg PO
PO daily daily
76-90 kg: 1600 mg 76-90 kg: 1600 mg PO
PO daily daily
Isoniazid 5mg/kg/day <15 years and ≤40 kg:
10-15 mg/kg/day;
maximum dose: 300
mg/dose
<15 years and >40 kg
and ≥15 years: 5
mg/kg/day
Pyrazinamide <40 kg: 35 mg/kg/day 40-55 kg: 1000 mg daily
40-55 kg: 1000 mg 56-75kg: 1500 mg daily
daily
56-75 kg: 1500 mg 76-90kg: 2000 mg daily
daily
76-90 kg: 2000 mg
daily
Rifampin/rifampicin 10 mg/kg once daily 10 to 20 mg/kg once
daily
(maximum: 600 (maximum: 600 mg/dose)
mg/dose)
11
Head CT if Indicated
In patients where there is a moderate to high suspicion of CNS infection and the lumbar
puncture has not yet been done, parenteral anti-infectives SHOULD NOT BE DELAYED while
waiting for a CT scan. CSF sterilization occurs only after 4-6 hours in the most sensitive
organisms, and patient outcomes are linked to earlier antibiotic treatment. Therefore,
presumptive treatment in a patient who later has a normal LP is far better than waiting to give
antibiotics for the CT, then LP results confirm bacterial meningitis.
A head CT is NOT always required prior to an LP. The logic of performing a head CT prior to
LP is to prevent cerebral herniation from an intracranial mass lesion. In this setting, lowering
lumbar pressure could cause downward herniation of the brain.
Indications for neuroimaging prior to lumbar puncture:

✓ Patient is ≥ 60 years
✓ History of CNS disease
✓ Immunocompromised state
✓ History of seizure (within one week of presentation)
✓ Abnormal neurologic exam findings
o Impaired level of consciousness
o Abnormal language
o Cranial nerve findings
o Motor findings
o Papilledema or loss of venous pulsations on fundoscopic examination
A normal head CT does not necessarily protect the patient form a herniation syndrome. Brain
herniation after LP occurs in approximately 5% of cases or less. CT scan can detect brain shift
and findings of impending herniation, contraindicating an LP. However, CSF pressure may be
elevated, even to levels where herniation may occur, in absence of abnormalities on CT.
Meningitis can be fulminant and characterized by progressive inflammation of the meninges
and brain swelling. Patients can herniate after LP because of disease progression, or due to
the inflammatory response to bacterial proinflammatory substances liberated after antibiotic
administration (especially if steroids are not given around the time of first antibiotic
administration), and not necessarily as a result of the LP. Vice versa, CSF pressure can be
normal in patients with space occupying lesions causing brain shift seen on CT scan, even in
the stage of herniation, and the LP may lead to herniation even with the CSF having normal
pressure.
In a patient with none of the above indications, doing an LP prior to head imaging is likely safe.
However, in most patients who have a clinical presentation consistent with meningitis or
encephalitis, there will be enough diagnostic uncertainty that CT may be advisable prior to LP
to rule out other etiologies.
If the head CT shows a mass lesion or other condition that adequately explains the patient's
mental status, then that cause should be diagnostically evaluated and LP avoided.
12
Lumbar Puncture
Rapid assessment of spinal fluid
An LP is essential for both establishing a diagnosis and tailoring therapy.
The opening pressure should be measured with a manometer prior to the collection of CSF in
the left lateral decubitus position. CSF should be collected in (at least) 4 tubes.
• Send tube 1 and tube 4 for RBCs and WBC count and differential (if tube 1 was
turbid, and tube 4 is clear, this suggests a traumatic tap)
• Send tube 2 for protein, glucose, and lactic acid
• Send tube 3 for gram stain and culture; India ink if fungal infection is suspected;
antigens, PCR (For viruses, especially herpes viruses. May also be sent in tube 2),
IgM for viruses, viral culture
Some laboratories perform bacterial antigen assays which may be useful. Additional
laboratory tests that may be performed by some centers include bacterial PCR (particularly for
Mycobacterium), enterovirus PCR, fungal antigens and viral culture.
13
Normal LP
Rules out meningitis and encephalitis
An LP is considered normal if:
• No RBCs/HPF or up to ≤ 5
• WBCs ≤ 5/HPF
• CSF glucose/serum glucose ratio >0.6
• Protein < 50 mg/dl
• No organisms seen on gram stain
If all of the above are true, meningitis is ruled out. However, a normal LP may be consistent
with non-herpetic encephalitis, but other than medical support there is no emergency
intervention that is necessary. Evaluation for systemic infection should also ensue.
Evaluate for Other Diagnoses

A normal LP is highly predictive of absent bacterial infection of the meninges. Pure
encephalitis, and perhaps early herpes simplex encephalitis, can have a normal lumbar
puncture since the inflammation is within the brain parenchyma and may not communicate with
the subarachnoid space. However, given the constellation of fever, leukocytosis and altered
mental status, it is likely the patient is suffering a depressed mental status from systemic
inflammation rather than direct involvement of the central nervous system itself.
This is termed “metabolic encephalopathy” and is common in patients with preexisting brain
disorders or atrophy. Once the true infection is found and treated (urinary tract, lungs, sepsis),
the patient’s mental status improves to baseline. Prolonged poor mental status after systemic
signs of treatment appear (defervescence, falling WBC count) may prompt additional
investigation as to cause.
14
Very High WBCs
WBCs > 100-1000
Marked elevation in WBCs without RBCs is highly suggestive of bacterial meningitis. So, if the
following is true:
• No RBC
• WBCs 100-1000/HPF or higher
• CSF glucose/serum glucose ratio <0.6, but rarely normal
• Protein > 50 mg/dl
• Organisms seen on gram stain in approximately 70% of cases
Then, the patient likely has bacterial meningitis.
Suspicion of Bacterial Meningitis

• Continue antibiotics
• Stop acyclovir
• Continue dexamethasone
• Adjust antibiotics, and either continue or stop dexamethasone based on final culture
results, and sensitivities.
In addition to antibiotics and dexamethasone, supportive care and management of other

systems is important in patients with bacterial meningitis. Some patients may have a
concomitant bloodstream infection with the offending pathogen and may require early goal
directed therapy for sepsis. If the LP demonstrates an elevated OP, ICP monitoring and
treatment of intracranial hypertension may be required. Details of management of intracranial
hypertension can be found in the ENLS manuscript on the same topic and in the 2019
Neurocritical Care Society Guidelines for Cerebral Edema Management. Risks, including the
potential of a superinfection with the foreign body, must be weighed with the potential benefits.
If the OP is found to be greatly elevated (e.g., > 400 mm H2O), expert opinion recommends
that the needle stylet should be left in place and mannitol administered. It may be prudent to
recheck the pressure after a few minutes to confirm that the CSF pressure has declined,
before removing the needle. Hyperventilation should probably be avoided as these patients
already may suffer from some degree of decreased cerebral vessel diameter due to
vasculopathy. Mannitol or hypertonic saline may be reasonable considerations.
Age factors:
• Neonates have a permeable blood brain barrier and are at risk of infection caused
by Group B streptococcus (GBS), Listeria monocytogenes, and Escherichia coli.
Empiric antibiotic therapy should include ampicillin, gentamicin and a third
generation cephalosporin (ceftazidime or cefotaxime). Cefotaxime is currently not
available in the US.
15
• Infants, children, and young adults with suspected bacterial meningitis are at risk for
Haemophilus influenzae (if not vaccinated), Neisseria meningitidis, and
Streptococcus pneumoniae. As such, they should be started on a 3rd generation
cephalosporin and vancomycin at doses appropriate for CNS penetration.
• Middle-aged adults are at highest risk for Streptococcus pneumoniae. As such, they
should be started on a 3rd generation cephalosporin and vancomycin at doses
appropriate for CNS penetration.
• The elderly and immunosuppressed are at risk for Streptococcus pneumoniae and
Listeria monocytogenes. As such, they should be started on ampicillin, a 3rd
generation cephalosporin and vancomycin at doses appropriate for CNS
penetration.
• In case of severe penicillin allergy, vancomycin can be used for gram-positives with
moxifloxacin or levofloxacin for S. Pneumoniae, N. Meningitidis, H. influenzae.
Trimethoprim-sulfamethoxazole is used when Listeria is suspected, and aztreonam
may be used for Gram-negative coverage.
16
Elevated WBCs and no RBCs
Probably viral meningitis
Mild elevation in WBCs without RBCs is suggestive of viral meningitis or viral (not herpes)
encephalitis. If the following is true:
• No RBC per HPF

• WBCs 10-100s
• Normal CSF glucose/serum glucose ratio (>0.6)
• Protein < 50 mg/dl (if elevated, it is usually <100 mg/dL)
• No organisms seen on gram stain
Then the patient likely has a non-herpes viral meningitis or encephalitis.

Seroconversion of HIV should also be considered.
Viral meningitis or viral (non-herpes) encephalitis treatment

Treatment of viral meningitis or viral (non-herpes) encephalitis:
• Discontinue acyclovir and antibiotics
• Discontinue dexamethasone
• Treat headache
• For West Nile Virus, there is risk of respiratory decompensation from spinal cord
involvement so admission to the ICU for observation may be appropriate
17
Elevated WBCs and RBCs
Consider herpes encephalitis
If the following is true:
• Elevated RBC (10–100/HPF or higher),

• WBCs in the hundreds/HPF, typically with lymphocytic predominance,
• CSF glucose/serum glucose ratio >0.6, or sometimes lower,
• Protein < 50 mg/dL or mildly elevated usually <100 mg/dL, and
• No organisms on gram stain,
then the patient may have herpes encephalitis. The presence of seizures and findings of uni-
or bilateral hypodensities with or without hemorrhage in the temporal lobes on brain MRI, and
rarely on brain CT scans, are also compatible with this diagnosis.
Empirical treatment and diagnosis of herpes encephalitis

• Continue acyclovir 10 mg/kg every 8 hours IV
• Send CSF for HSV PCR
• Continue other antibiotics until cultures/PCR results back
• MRI of the brain
• Achieve and maintain euvolemia to prevent acyclovir associated renal failure
18
Elevated WBCs and Very High Total Protein
Fungal or TB Meningitis
Fungal CNS infections are highly variable in clinical presentation and need to be considered in
suspected CNS infections that evolve over days in an immunosuppressed patient. Prior
history of CNS disease or systemic fungal infections and rapid disease progression should
raise the index of suspicion for fungal meningitis.
As with other CNS infections, fast identification and treatment initiation significantly affects the
odds of a better outcome. Typical CSF findings include lymphocytic pleocytosis (few to several
hundred per HPF) and for certain organisms also with eosinophilic predominance. CSF
glucose is decreased, and CSF protein is generally elevated (up to 250 mg/dl or beyond). If
CSF acquisition via LP is difficult or impossible, it can be an indicator of very high (>1 gm/dL)
CSF protein and obstructive hydrocephalus. Empiric amphotericin B should be administered
during diagnostic testing.
19
Elevated RBCs, Xanthochromia

Likely Subarachnoid Hemorrhage
If the following is true:
• Elevated RBC (100 to 1,000/HPF or higher),

• WBC < 5/HPF or fewer than 1 WBC/500 RBC,
• CSF glucose/serum glucose ratio >0.6,
• Protein < 50 mg/dl,
• No organisms on gram stain, and
• Xanthochromia,
then the patient likely has a subarachnoid hemorrhage that was not detected on the CT scan.
Xanthochromia may be absent if the LP was done within the first few hours of headache onset
(and so one typically only sees RBCs).
Management of SAH
Review the head CT to look for subarachnoid blood (this can be absent after SAH
approximately 5% of the time, particularly with small hemorrhages and imaging obtained long
after symptom onset).
See the ENLS protocol Subarachnoid Hemorrhage.
20
Resuscitation Following Cardiac
Arrest Protocol
Version 4.0
Authors
Sarah Livesay, DNP, APRN, ACNP-BC, ACNS-BC
Matthew Kirschen, MD, PhD
Sarah Peacock, DNP, APRN. ACNP-BC
Jonathan Elmer, MD, MS

Sarah Livesay, DNP, APRN
Jonathan Elmer, MD, MS
Resuscitation Following Cardiac Arrest Algorithm

Resuscitation Following Cardiac Arrest Protocol
Checklist
☐ Initiate hemodynamic and ventilator support
☐ Assess for common treatable causes of arrest, consider coronary angiography
☐ Assess eligibility for targeted temperature management
☐ Begin induction to target temperature
☐ Consider transfer to specialty center
Communication
☐ Patient age, pre-arrest circumstances
☐ Duration of CA and initial arrest rhythm
☐ Most likely etiology of arrest, if known
☐ Neurological examination on first assessment
☐ PCI eligibility
☐ Time hypothermia started and/or target temperature reached
☐ Current core temperature
☐ Current drug infusions (especially sedative and vasoactive agents)
Sample Sign-off Narrative
Prehospital to ER:
I am signing out a 58-year-old man with known hypertension who collapsed with co-workers
while walking to lunch. CPR was started by co-workers, an AED was applied and patient found
to have a shockable rhythm. He was shocked once by the AED. EMS arrived approximately 10
min later. He was found to be in ventricular tachycardia, and he received 1 mg of epinephrine
and was shocked again. ROSC after approximately 18 min. After ROSC, we obtained an EKG
and the patient was found to have ST elevation in leads V3-V6. He has an LMA and oxygen
saturation is 100%. Blood pressure is 130/85 mm Hg and he is now in sinus tachycardia at 108
beats/min.
ER to ICU:
58-year-old man with out of hospital CA with ROSC obtained at 18 min. He was found to have
a STEMI and underwent PCI with stenting of a proximal LAD occlusion. He received heparin,
aspirin, and prasugrel in the cath lab. On his initial neurological examination post-cath GCS
was 5 (E1V1M3). TTM was started with a target temperature of 36 °C. Target temperature was
achieved 45 min later at 14:10. Current temperature is 36.1 °C with a gel adhesive pad cooling
device applied. The patient is currently on 2mcg/kg/min of norepinephrine. He received a
single dose of cisatracurium at the initiation of TTM with 2gm of magnesium and 150mcg of
fentanyl. Fentanyl is ordered PRN for shivering along with the TTM and shivering management
order set.
3
Anticipate and Prepare for Potential Rearrest

Patients resuscitated from cardiac arrest are among the sickest encountered by most intensive
care providers. During and immediately after a cardiac arrest, several parallel workflows are
necessary to support successful resuscitation. Concurrently with CPR and stabilization,
providers should diligently search for the underlying etiology of arrest. In parallel with
cardiopulmonary stabilization, efforts must be taken to minimize the risk of secondary brain
injury. Patient who remain comatose following return of spontaneous circulation are likely to
benefit from targeted temperature management. They may also benefit from transfer to
specialty care. This protocol addresses initial patient stabilization and assessment, induction
of targeted temperature management in eligible patients, and shivering management. This
protocol does not address the standard ACLS protocols for cardiac resuscitation.
- Approximately 20% of patients rearrest within minutes of initial restoration of pulses.

- Even without frank rearrest, anticipate the likelihood of hemodynamic instability.
- Patients resuscitated from cardiac arrest typically require intubation, mechanical
ventilation, close cardiac and invasive hemodynamic monitoring, and attentive general
critical care.
- Many patients will require titration of fluids, vasopressors, administration of
antidysrhythmics, etc., in the minutes after initial resuscitation.
- Blood pressure and oxygenation goals should be chosen to maintain cerebral perfusion
and prevent secondary brain injury.
4
Identify Reversible Etiologies of Arrest

- Concurrently with CPR and stabilization, providers should diligently search for the
underlying etiology of arrest
- Diagnostic evaluation after ROSC may include a focused history, physical examination,
electrocardiogram (EKG) and judicious imaging, and prioritize identification of those
etiologies that require specific time-sensitive interventions beyond general resuscitative
measures.
- Specific etiologies of arrest requiring emergent treatment include:
- Acute coronary syndrome/myocardial infarction
- Arrhythmia
- Intracranial hemorrhage
- Pulmonary embolism
- Trauma
- Hemorrhage (e.g. GI bleed)
- Toxicological causes/overdose
- Septic shock
- Anaphylaxis
5
Hemodynamic Support
Maintain
- Identify and treat hypotension and keep MAP >80 mmHg

- Volume resuscitation and blood pressure goals with cerebral perfusion and prevention
of secondary brain injury in mind
- Rapid PCI when patient is identified as a candidate for intervention
6
Pulmonary Management
- Secure airway
- Temperature correct ABG while patient is on TTM
- Rapidly identify and correct hypoxia
- Maintain PaO2 80-120 mmHg
- Maintain PaCO2 ≥ 40 mmHg
- Avoid hyperoxia
7
Evaluate for Immediate Coronary Intervention

Does the patient need coronary intervention?
- Coronary angiography should be considered for patients with clinical suspicion for an
acute coronary syndrome based on EKG (e.g. ST segment changes) or history (e.g.
initial shockable rhythm, no other obvious etiology of arrest).
- TTM is not a contraindication for coronary angiography.
- Patients with initial evidence of devastating brain injury (e.g. diffuse cerebral edema on
initial brain imaging) are unlikely to benefit from coronary revascularization.
8
If Eligible for Targeted Temperature Management

Rapid induction to 33-36°C
The patient is eligible for TTM if she/he:

- Suffered a cardiac arrest
- Has return of spontaneous circulation
- Does not follow commands.
- Choose target temperature (33-36°C)
Absolute contraindications:
- DNR/POLST indicating they would not want this level of treatment
- Following commands
If no absolute contraindications, consider the following minor contraindications when

determining what temperature to target in each individual patient:
TTM at 36°C is preferred in case of:

- Active bleeding with the cause not (yet) under control
- Greatly increased risk of bleeding (e.g. injury of the spleen or liver)
- Traumatic etiology of cardiac arrest
- Anticipated hemorrhagic diathesis
- Cardiac arrest more than 12 hours ago
After considering risks and benefits:

- Set Target Temperature to 33°C or 36.0°C
If eligible for TTM: rapid induction to 33-36°C

- Core temperature monitoring
- Combine several cooling induction methods, particularly if targeting 33°C, including
cold saline and application of temperature control device*
- Sedation
- Monitor for and management of shivering
*Cold saline is not recommended in the prehospital setting
9
Shiver Management
- Monitor for shivering
- Treat shivering when present using a multi-modal approach
- Skin counter-warming
- Acetaminophen, magnesium, sedation
- Intermittent dosing of paralytics may be considered if shivering is refractory to
other treatment
- See ENLS protocol Pharmacotherapy-Shivering Protocol
10
Consider Transfer to Specialty Care

- Post-arrest patients cared for at high-volume centers have improved short- and long-
term outcomes.
- Transfer of comatose post-arrest patients to a specialty center offering PCI, cardiac
critical care, TTM, and neurocritical care may be prudent.
- Active engagement of a critical care transport physician should be considered when
arranging interfacility transport of unstable patients resuscitated from cardiac arrest to
ensure adequate resources are mobilized for patient transport.
11
Spinal Cord Compression Protocol
Version 4.0
Authors
Ryan Martin, MD
Sarah Peacock, DNP, APRN. ACNP-BC
Megan Corry, EdD, EMTP
Kerri L. LaRovere, MD
Safdar A. Ansari, MD

Spinal Cord Compression Algorithm

Checklist
☐ Brief history of the patient
☐ Spinal motion restriction (motion restriction)
☐ Ensure proper ventilation, especially in the presence of quadriplegia
☐ Labs: CBC, Chemistries, INR/PT, PTT, platelet function assay (e.g. VerifyNow
platelet reactivity profile)
☐ Obtain emergent spine imaging (MRI unless contraindicated)
☐ Alert spine surgeon
☐ Suspected neoplastic disease: administer corticosteroids (dexamethasone 10 mg IV
load and 4 mg every 6 hours IV/PO), contact radiation oncology
☐ Suspected epidural infection: check ESR and start antibiotics
☐ Initiate interfacility transfer if anything cannot be performed at your facility
Communication
☐ Age, gender, premorbid conditions and risk factors
☐ Onset and duration of symptoms
☐ Paraplegia or quadriplegia
☐ Spinal level of clinical involvement
☐ Vital signs
☐ Airway status
☐ Bowel or bladder involvement
☐ Results of lab tests
☐ Results of imaging studies, if available
☐ Medical history (i.e. cancer, intravenous drug abuse, immunosuppression)
☐ Therapies initiated
☐ Discuss further interventions to start now
Sample Sign-off Narrative:

“I am transferring to you a patient who I suspect has a spinal cord compression secondary to
an epidural abscess.
He is a 67-year-old male with a history of hypertension, diabetes, and intermittent intravenous
drug use who presented one hour ago with mid-back pain over the last two weeks.
Over the last four days, his legs have been weak, and today he was unable to walk.
He appears paraplegic with a T-10 sensory level.
He has had low-grade fevers and chills since his back pain started.
On exam, he is afebrile, blood pressure is within normal limits and he has no evidence of
respiratory insufficiency.
Strength in his arms is normal, but he is unable to lift his legs off the bed.
His bladder was distended and a Foley was placed.
CBC and coags are normal. ESR is pending. We do not have any spinal imaging available.
3
Given his history of IV drug use and recent fevers and chills, we suspect this is an epidural
abscess leading to spinal cord compression.
Empirical antibiotics were started, including vancomycin, ceftriaxone and metronidazole.
We are initiating transfer to your facility for emergent MRI of the spine and surgical
consultation.
Is there anything else we should do before transfer?”
4
Acute Disc Herniation

Decompression
If imaging reveals compression from disk herniation or from bone/vertebral body encroachment
(spinal stenosis):
• Disk herniation that compresses the spinal cord or the cauda equina may represent
a neurosurgical emergency.
• Disc herniation that does not compress the spinal cord or cauda equina is less
urgent.
5
Acute Hemorrhage
Reverse coagulopathy and decompression
Spinal hematomas can present with rapidly developing paraparesis or quadriparesis with local
or radicular pain. Spinal epidural hematomas are the more common compressive etiology, but
intra-medullary hemorrhage (hematomyelia) can also occur and presents similarly. The most
common causes of non-traumatic spinal cord hematoma include vascular malformations,
coagulopathy, inflammatory myelitis, spinal tumors, and syringomyelia. Traumatic causes
include penetrating injuries and high-impact, blunt-force trauma, or may be iatrogenic as a
result of post-surgical bleeding. In rare cases, spinal hematoma can be a late complication
after radiotherapy, presumably due to bleeding from telangiectasia caused by the radiotherapy.
MRI with and without gadolinium is the modality of choice for diagnosing spinal hematoma, as
it will demonstrate both the hematoma and any associated underlying pathology, including
spinal cord edema.
Treatment includes rapid reversal of coagulopathy and evaluation for surgical decompression.
6
Assess Airway and Hemodynamics
Cervical myelopathy may affect diaphragm
Those patients with quadriplegia should be monitored closely for respiratory distress and
failure.
• Frequent bedside pulmonary function testing and the detection of dysphonia and
tachypnea are vital to diagnose impending respiratory collapse.
• Consider intubation if:
▪ Negative Inspiratory Force (NIF) < -30 cmH2O
▪ Forced Vital Capacity (FVC) < 1L
• The patient’s own assessment of their respiratory status is frequently accurate but
may be unreliable in the presence of analgesia or sedation.
• A low threshold should be maintained for placement of a definitive airway and
mechanical ventilation, particularly if rapid progression of motor weakness is
observed
If there is any suspicion of trauma, do not extend the spine for intubation, and refer to the
ENLS protocol for Traumatic Spine Injury.
For patients with total body weakness and cranial nerve deficits, consider a generalized
neuromuscular disorder, or a stroke. Secure the airway first, then pursue the ENLS protocol
for Acute Non-Traumatic Weakness, or the ENLS protocol for Acute Ischemic Stroke.
Once ventilation has been assessed, move on to acute imaging, but for those patients who are
not intubated, anticipate progression of weakness and ensure continuous monitoring of
ventilation as the work-up continues.
7
Corticosteroids
Empirical treatment if cancer is suspected
Patients with malignant SCC and acute neurologic dysfunction should receive corticosteroids.
Empirical treatment with corticosteroids is recommended in patients with known malignancy
and acute SCC, even if unconfirmed by MRI spine imaging.
• Steroids are often given to rapidly reduce edema and decrease the chance of spinal
cord venous infarction. The use of steroids in patients with compression from
epidural metastatic disease is considered to be part of standard medical therapy.
• Given the safety profile and efficacy of the lower dose of dexamethasone, we
recommend a dexamethasone 10 mg IV loading dose followed by 4 mg oral/IV every
6 hours as maintenance.
8
Emergent Transfer
To a facility that has spine imaging available
Due to the rapid progression of some acute SCC syndromes, transfer agreements between
emergency departments and other acute care facilities should be pre-established to avoid
prolonged attempts to find a facility when time is of the essence. Emergent transfer is
warranted when the acute care facility treating the SCC patient is unable to provide definitive
care.
If the circumstance arises in which there is no feasible way to transfer a patient, or if the
transfer will be delayed significantly, spinal motion should be restricted to prevent worsening of
spinal cord compression, and empirical treatment with corticosteroids or antibiotics for the
most likely diagnosis should be implemented without delay. The medical complications of
spinal cord injury will also need to be monitored and treated, including respiratory and
hemodyna.mic instability, constipation, urinary retention, pain, deep vein thrombosis, and
pressure ulcers
9
Empirical Antibiotics
Empirical treatment for presumed infectious cause
Patients with evidence of infection such as fever, leukocytosis, intravenous (IV) drug use, or a
known infectious source should be started on empirical antibiotics after blood and urine
cultures are drawn.
• Draw blood cultures and ESR

▪ An ESR of less than 20 has excellent sensitivity for excluding a diagnosis
of spinal epidural abscess
• Start empirical antibiotics with broad spectrum coverage
▪ Abscesses are often multi-microbial
▪ MRSA coverage – start vancomycin
▪ Gram negative coverage – start third or fourth generation cephalosporin
▪ Anaerobic coverage with metronidazole should be considered
10
Imaging Not Available
No MRI or CT
Without imaging, consider empirical medical treatment until imaging can be obtained.
• If the history, clinical picture suggests infection and epidural abscess is a possibility,
start empirical antibiotics.
• If there is a history of cancer and neoplastic spinal cord compression is a possibility,
start empirical corticosteroids.
• Expedited transfer to a facility with imaging capability is necessary.
11
Infectious Lesion
Empirical antibiotics and ESR
Suppurative infections of the spinal epidural space can cause neurological injury directly by
compressing the spinal cord, or indirectly, by compromising blood flow. The classic triad of
fever, back pain, and neurologic dysfunction is not seen in most patients, and other symptoms
may include localized back pain, radiculopathy, weakness, sensory changes, and sphincter
dysfunction.
• STAT consultation with a spine surgeon or facilitation of transfer if none is available.

• Draw blood cultures and ESR
▪ An ESR of less than 20 has excellent sensitivity for excluding a diagnosis
of spinal epidural abscess
• Start empirical antibiotics with broad spectrum coverage
▪ Abscesses are often multi-microbial
▪ MRSA coverage – start vancomycin
▪ Gram negative coverage – start third or fourth generation cephalosporin
▪ Anaerobic coverage with metronidazole should be considered
• Antibiotics alone (without decompression) may be considered in patients who are
either neurologically intact or who have had complete weakness for more than 48-72
hours.
▪ In these patients, close observation for neurological worsening is advised
given the high failure rates of medical management (6-49%)
▪ Risk factors for neurological worsening
• Diabetes
• CRP > 115
• WBC > 12
• age > 65
• positive blood cultures
• MRSA infection
• In patients with neurological deficits, early decompression, irrigation, and
debridement is the mainstay of treatment [49].
12
MRI Spine
Spine imaging is available
Emergent MRI with gadolinium is preferred in most cases.
• CT with contrast and or CT myelogram is an alternative if MRI is contraindicated or

not available.
Imaging is used to rule out any compressive etiology of the spinal cord like tumor, infection, or
intervertebral disc herniation. It is important to communicate the neurological findings to your
radiologist so that the proper location(s) of relevance are imaged.
• Quadriplegic patients should have at least the C-Spine imaged. Entire spine
imaging (including the conus) may also be appropriate especially if the patient has
known cancer.
• Paraplegic patients (if there are no symptoms in the arms) should have thoracic and
lumbosacral spine imaged.
• A discussion with the radiologist is important to image the proper level, and to
expedite the imaging so that treatments can be provided efficiently and quickly.
• It is also important to notify a spine surgeon that your patient may have a
myelopathy that will need surgical decompression, and when their spine imaging will
be completed.
13
Negative Imaging or Intrinsic Spinal Cord Lesion
ENLS Non-traumatic Weakness Protocol
Patients with acute symptoms of spinal cord dysfunction can have intrinsic or intra-medullary
(non-compressive) abnormalities of the spinal cord on MRI. These include spinal infarct,
inflammatory / demyelinating myelitis, infectious, and para-infectious disease.
Spinal cord ischemia may require further imaging with spinal angiography to identify
arteriovenous malformation, arterial occlusion or other vascular abnormalities. Serum and
CSF studies should be sent for evidence of autoimmune and infectious vasculitis. Serum
studies should include serology for Lyme, syphilis, human immunodeficiency virus (HIV), and
nutritional deficiencies including vitamin B12. CSF should be tested for viral studies including:
herpes simplex virus 1,2 polymerase chain reaction (HSV PCR), cytomegalovirus (CMV) PCR,
and Varicella Zoster Virus (VZV) IgM and IgG. Immunoglobulin indices should be evaluated
including (but not limited to): IgG index, Albumin index, IgG synthesis rate and oligoclonal
bands. Urine should be screened for copper deficiency (see the ENLS Acute Non-Traumatic
Weakness protocol).
Negative spinal MRI in a patient with acute disturbance of motor and or sensory function
(quadriplegia or paraplegia) should prompt evaluation for acute neuropathy, neuromuscular
junction disorders and myopathy. Clinical presentation, CSF, and electrophysiologic studies
may establish a diagnosis of Guillain-Barre syndrome (acute polyradiculoneuropathy),
Myasthenia Gravis, Lambert-Eaton syndrome, or motor neuron disease (see ENLS Acute
Non-Traumatic Weakness protocol).
Spinal cord injury without radiographic abnormality (SCIWORA) is a clinical diagnosis made in
the setting of trauma and spinal cord dysfunction without an MRI abnormality. The cervical
spinal cord is most likely affected due to increased mobility of the cervical spine. Children are
high risk for this injury due to the relatively large head-to-body ratio in childhood. Treatment is
non-surgical due to the absence of a surgical lesion. Supportive measures include spinal
motion restriction with collars, braces, or orthosis for up to 3 months. The use of corticosteroids
in this setting should be carefully evaluated with inherent risks and used judiciously.
14
Neoplastic Disease
Steroids, decompression, radiation oncology
Patients with malignant SCC and acute neurologic dysfunction should receive corticosteroids.
Empirical treatment with corticosteroids is recommended when malignant SCC is suspected,
even if unconfirmed by MRI spine imaging.
• Steroids are often given to rapidly reduce edema and decrease the chance of spinal
cord venous infarction. The use of steroids in patients with compression from
epidural metastatic disease is considered to be part of standard medical therapy.
• Given the safety profile and efficacy of the lower dose of dexamethasone, we
recommend a dexamethasone 10 mg IV loading dose followed by 4 mg oral/IV every
6 hours as maintenance.
Once imaging and diagnosis is confirmed, a combination of surgical treatment, radiotherapy,

and chemotherapy is recommended. Surgical removal of tumor and spinal decompression is
the primary and emergent treatment for malignant SCC.
• Early surgery (within 24 hours) with circumferential removal of the tumor,

decompression of the spinal cord, and stabilization of the spine has been shown to
significantly improve clinical outcomes (ambulation and pain), quality of life, and
reduces need for narcotics and corticosteroids. It is also associated with a trend
towards improved survival rate.
Radiotherapy is often used in conjunction with surgery and is also recommended alone in
patients with minimal neurologic dysfunction and high degree of tumor responsiveness to
radiation. Hematologic tumors such as lymphoma, myeloma, and seminoma are highly
radiosensitive, while breast, lung and prostate have intermediate radiosensitivity. There have
been significant advancements in radiosurgical techniques, and all malignant SCC patients
should be referred for evaluation.
Chemotherapy is not a mainstay for acute treatment of malignant SCC and is always delivered
in conjunction with radiotherapy and surgery.
15
Paraplegia
Paralysis of the legs and lower body. This typically related to compression of the thoracic
and/or lumbar spine.
Ventilatory issues are uncommon in patients with paraplegia/paraparesis, and transport and
MRI imaging are safe.
16
Quadriplegia
Special airway issues
In the event of sudden or progressive quadriparesis or quadriplegia, the cause may be a

cervical cord pathology. This may lead to hypoventilation because of both chest wall and
diaphragmatic weakness, and respiratory assessment is vital before transport or MRI imaging.
Ventilatory issues are uncommon in patients with paraplegia/paraparesis, and transport and
MRI imaging are safe.
17
Spinal Cord Compression
Suspected myelopathy
The presentation of spinal cord compression includes:
• Back/neck pain
• Bilateral weakness or paralysis of the limbs
• Urinary retention
• Obstipation
• Sensory level
▪ Defined as a loss of sensation below the dermatomal level of
compression.
• Spinal shock
▪ Defined as flaccid paralysis, loss of reflexes, and sensation below the
level of compression
• Compression of the cauda equina can cause a similar clinical presentation with
concomitant perineal (saddle) anesthesia and radicular pain
• Spinal cord compression at or above T4 can lead to hemodynamic instability
secondary to loss of sympathetic tone
▪ This leads to neurogenic shock with systemic hypotension and relative
bradycardia
SCC of the cervical segments can lead to quadriplegia, whereas compression below these
levels causes paraplegia, which is far more common. Quadriplegia is the most disabling
presentation of SCC, and when present in an alert and responsive patient, should suggest a
cervical spinal cord lesion. The most widely used severity scale is the American Spinal Injury
Association Impairment Scale (ASIA) which was devised for traumatic SCC.
Immediately after recognition or suspicion for SCC, spinal motion restriction should be
instituted with a cervical collar and thoracolumbar motion restriction if warranted. Spinal motion
restriction and precautions during patient care (and transport) prevent further cord
compression and injury. While optimal blood pressure is not known, spinal cord blood flow is
often impaired in the setting of a compressive lesion, and hypotension should be avoided.
18
Suspicion of Cancer
Possible metastasis
Consider spinal metastasis with spinal cord compression if there is a history of cancer, or new
suspicion of cancer.
19
Suspicion of Infection
Consider epidural abscess
Suspicion for an infectious cause (epidural abscess) rises if the following are present:
• Fever
• Elevated WBC count
• Elevated ESR
• History of intravenous drug use
• Known infectious source- current or past endocarditis, sepsis, chronic infection like
osteomyelitis
• Any of the above with focal spine tenderness elicited by percussion (reflex hammer
striking your finger placed over the vertebral spinous process)
20
Subarachnoid Hemorrhage Protocol
Version 4.0
Authors
Sayona John, MD
Stephanie Qualls, RN, BSN, CNRN
Brian L. Edlow, MD
Last updated:
October 2019

Sayona John, MD
Brian L. Edlow, MD
Subarachnoid Hemorrhage Algorithm

Checklist
☐ Airway, breathing, circulation
☐ Head computed tomography (CT)
☐ Laboratories: PT/INR, PTT, CBC, chemistries, troponin, toxicology screen
☐ 12 lead ECG
☐ Target SBP goal < 160 mmHg
☐ Consult neurosurgery/NCC team
☐ Address hydrocephalus if present
Communication
☐ Airway status
☐ Hemodynamic status and blood pressure control (BP goals)
☐ Clinical presentation (level of consciousness, motor examination, pupils)
☐ WFNS score and Hunt–Hess Grade
☐ Imaging/LP results
☐ Coagulopathy present?
☐ Hydrocephalus present?
☐ Medications given (dose and time administered), including sedatives, analgesics, seizure
prophylaxis, anti-hypertensives, and nimodipine
☐ Coordination of other vascular imaging
Sample sign off narrative:

“I am signing out a 45-year-old man with no known past medical history”
“He complained of a severe headache and was then found unresponsive at his work place at 3
PM, last seen normal by his coworker at 2:45 PM. GCS in
the field was 9, and BP was 180/110”
“On arrival to the ED here, he was the same, so we drew labs and sent him for a head CT”
“CT completed at 4:30 PM showed a diffuse subarachnoid hemorrhage, minimal
intraventricular hemorrhage with mild hydrocephalus. CTA shows a right anterior
communicating artery measuring 7 mm”
“When he returned to the ED, he was sleepier, with a GCS of 5, so he was intubated using
rocuronium and etomidate”
“His labs came back with a Troponin of 0.9 and ECG with diffuse T wave inversions. His chest
x-ray reveals mild volume overload”
“Neurosurgery has been called, and they are on their way to see him. He is in ED
Resuscitation Room 3, intubated and sedated now on propofol at 30
mcg/kg/min and fentanyl 50 mcg/h. His BP is 140/80 with no other treatment”
“They are ready to take him in Bed 12 in the NCCU in 5 min. Nursing is also calling report”
3
Subarachnoid Hemorrhage (SAH)
Blood within the subarachnoid space
Subarachnoid Hemorrhage (SAH) is most commonly produced by trauma and next most
common by a ruptured intracranial aneurysm. For the latter, it is imperative that a timely
diagnosis is made because the prevention of aneurysm re-rupture can be lifesaving.
4
Clinical Diagnosis of Subarachnoid Hemorrhage (SAH)
Clinical features
The diagnosis of traumatic SAH is based on history and brain imaging. The protocol for
management of traumatic SAH can be found under the ENLS protocol Traumatic Brain Injury.
Aneurysmal SAH has a classic presentation though signs and symptoms may vary.
Classic presentation:
• Abrupt onset of a sudden, severe headache; onset is typically less than 1 minute.
• The headache is a NEW, QUALITATIVELY DIFFERENT headache for the patient.
• May have neck pain, nausea and vomiting.
• The patient may transiently lose consciousness, or present in coma.
• The nature and onset of the headache is the key distinguishing feature from other
forms of stroke, syncope, and seizure.
Variant presentation:
• Headache is not reported as abrupt (the patient may not remember the event well).
• Headache responds well to non-narcotic analgesics or “anti-migraine” medications.
• Headache resolves on its own within hours.
• Approximately 40% of patients with SAH will have a normal neurological
examination. They may or may not have meningismus (which may take time to
develop). They do not necessarily appear acutely ill.
Key aspects of the neurological examination:

• Glasgow Coma Scale (GCS)
• Pupil exam
• Fundoscopic exam for retinal hemorrhages
• Neck exam for meningismus
Determine the clinical severity of the SAH using one of the scales below:
World Federation of Neurological Societies (WFNS) scale:

Grade 1: GCS 15
Grade 2: GCS 13-15 without neurological deficit
Grade 3: GCS 13-15 with neurological deficit
Grade 4: GCS 7-12
Grade 5: GCS 3-6
5
Hunt-Hess Scale (increase by 1 grade for angiographic vasospasm or serious systemic
illness):
Grade 1. Asymptomatic, mild headache, slight nuchal rigidity
Grade 2. Moderate to severe headache, nuchal rigidity, no neurologic deficit other than
cranial nerve palsy
Grade 3. Drowsiness / confusion, mild focal neurologic deficit
Grade 4. Stupor, moderate-severe hemiparesis
Grade 5. Coma, decerebrate posturing
6
Airway
Assess need for intubation
Factors contributing to necessity of intubation include:

• Insufficient airway protection
• Hypoventilation
• Hypoxemia
• Expected decompensation during transport within hospital or to another hospital
See ENLS protocol Airway, Ventilation and Sedation.
7
Prehospital Care
A variety of prehospital neurological examination tools, including the Cincinnati Prehospital
Stroke Scale, Los Angeles Prehospital Stroke Screen, National Institutes of Health Stroke
Scale, Miami Emergency Neurological Deficit Scale, and Glasgow Coma Scale, are used by
emergency medical services personnel. For patients presenting with isolated headache who
are neurologically intact, there are no specific prehospital interventions, apart from
consideration of analgesics. For patients presenting with a headache and neurological deficits,
pre-notification of the ED staff about the neurological deficits and the finger stick glucose are
important first steps. Patients who are severely encephalopathic, comatose, or vomiting
repeatedly may need to have their airway controlled by tracheal intubation in the field. Care at
a certified comprehensive stroke center that can provide neurosurgical and endovascular
consultation is recommended.
See ENLS protocol Acute Ischemic Stroke for prehospital protocol pertaining to SAH and other
types of stroke.
8
Brain Imaging for SAH
If you suspect SAH by history, head imaging is the next step
Non-contrast CT imaging of the brain is the gold-standard for identifying SAH (Class1, LOE B).
• However, CT imaging is more sensitive in the first hours following a SAH and
becomes progressively less sensitive with the passage of time (so that by 3 days, it
is approximately 85% sensitive). Besides time, other reasons for a false negative
CT include anemia, low volume SAH and a technically poor scan.
• Some clinicians advocate for a CT angiogram (CTA) at the time of the CT scan to
look for an intracranial aneurysm. Although this is helpful if an aneurysm is seen,
the negative predictive value is less clear. One should not use a negative CTA
alone to rule out SAH.
• MRI is useful in patients who are imaged a few days following the SAH; specific
sequences can be used to image subarachnoid blood even several days later.
A CT image of an aneurysmal SAH is shown below:
9
CT Confirms SAH
Blood is seen on the CT scan
The diagnosis of SAH is confirmed and cerebrospinal fluid analysis is not necessary.
10
CT Scan is Negative - Perform Lumbar Puncture (LP) Next
Must perform an LP if the CT is negative
Recent data suggest that non-contrast CT imaging of the brain is close to 100% sensitive for
SAH if all of the following are true:
• The patient has a classic presentation with a thunderclap headache,
• The CT is done within 6 hours of headache onset,
• The patient is completely neurologically intact, and
• The CT is read by an attending radiologist (or someone with equivalent experience
reading brain CT scans)
If all of these criteria are met, clinicians can consider not doing an LP. The sensitivity of CT in
these patients is ~ 99.5% (may miss a SAH in 1-2 patients per 1,000 who fulfill all of these
criteria).
However, if these criteria are not met, one should perform an LP to determine if the patient has
a radiographically occult SAH.
The LP is done to look for xanthochromia. Xanthochromia is the staining of CSF by heme
breakdown products (chiefly bilirubin). It takes several hours for blood in the subarachnoid
space to break down, so the presence or absence of xanthochromia is time dependent.
• If the CSF shows xanthochromia, the diagnosis of SAH is confirmed (be careful if the
CSF protein exceeds 100 mg/dl as this can lead to a false positive).
• If the CSF is clear of RBCs and xanthochromia is absent, it is highly unlikely that the
patient had a subarachnoid hemorrhage. However, a rapidly expanding aneurysm
without subarachnoid rupture can present with a classic thunderclap headache, so if
you still suspect an aneurysm on clinical grounds, emergent neurosurgical
consultation is recommended.
In summary, the typical findings of SAH on cerebrospinal fluid analysis are:

• some RBCs
• < 5 WBCs
• WBC:RBC ratio 1:700
• Xanthochromia is present
• Minimal clearing of RBCs between tubes 1 and 4.
Note:
• The sensitivity of all tests for SAH are dependent upon the time from the bleed. CT
is more sensitive early and less so with time. RBCs in the spinal fluid is also more
likely to be seen early and will clear with time. Xanthochromia is absent early and
nearly always present by 12 hours after the bleed.
• Spectrophotometry is more sensitive (but much less specific) for xanthochromia than
is visual inspection (spin down CSF, compare to water in neutral light; see figure
below); however visual inspection is the only test available at most hospital labs.
11
Typical appearance of xanthochromia (left) compared to water (right). CSF is centrifuged first
to take any RBCs out of solution.
12
SAH is Confirmed
CT or LP evidence of SAH
Diagnosis of SAH is confirmed. The goal is to reduce the chance of aneurysm re-rupture and
expedite treatment of the aneurysm while preventing any medical complications.
13
Initial Orders
First steps
Once SAH is confirmed, in addition to the items outlined below (neurosurgical consultation,
seizure prophylaxis, reverse coagulopathy, treatment of anxiety and pain, and blood pressure
management):
• Bed rest with cardiac monitoring
• 12-lead electrocardiogram
• Labs
o Blood: CBC, coagulation tests (prothrombin time, partial thromboplastin time,
international normalized ratio), electrolytes, renal function tests, troponin, and a
type and screen
o Urine: toxicology screen
14
Neurosurgical Consultation
Definitive therapy is obliteration of the aneurysm, by either endovascular coiling or surgical
clipping. Both of these therapies isolate the aneurysm from the cerebrovascular circulation and
should be carried out as soon as feasible, ideally within the first 24 h of presentation.
15
Seizure Prophylaxis
Should one prescribe anticonvulsants now?
• Approximately 20% of SAH patients have seizures prior to hospital arrival, and another
5–10% experience seizures after admission.
• Early seizures may increase the risk of aneurysm re-rupture and elevated intracranial
pressure (ICP).
• Acute seizures should be treated with antiseizure medications.
• In patients with persistent altered mental status, non-convulsive status epilepticus may
be present, which can only be diagnosed by continuous electroencephalography (EEG).
• Both the AHA and NCS guidelines suggest consideration of antiseizure medications in
the immediate post-hemorrhage period.
• A very short course of prophylactic antiseizure medications may be recommended in
the period following diagnosis and before definitive aneurysm treatment because of a
concern for seizure-related aneurysm re-rupture.
• As phenytoin may lead to worse long-term cognitive outcomes, the use of a different
agent should be considered. Refer to ENLS Pharmacology module for more
information.
16
Reverse Coagulopathy
Coagulopathy should be urgently treated.
• Patients taking Vitamin K antagonists including warfarin with an INR ≥ 1.4 should be
treated with some combination of IV vitamin K (10 mg IV), and prothrombin complex
concentrates.
• Fresh Frozen Plasma (FFP) is an alternative for reversal if PCC is unavailable.
• Thrombocytopenia (platelets < 100,000) can be treated with platelet transfusions.
See the ENLS Pharmacology protocol regarding reversal of Factor Xa and thrombin inhibitors.
For patients with SAH taking oral anti-platelet agents, such as aspirin, clopidogrel or prasugrel,
NCS and SCCM management recommendations include:
• Anti-platelet agents can potentially increase the risk and severity of aneurysm re-
rupture, as well as neurosurgical complications.
• Platelet transfusion is recommended for patients with aspirin- or adenosine diphosphate
(ADP) inhibitor-associated SAH who will undergo a neurosurgical procedure.
• Platelet transfusion is not recommended if no neurosurgical procedure is planned.
• The risk–benefit ratio of anti-platelet therapy reversal using other hemostatic agents
such as desmopressin (DDAVP) should be considered for individual patients.
17
Treat Pain and Anxiety

An uncomfortable patient can re-rupture his or her aneurysm
It is important to avoid straining, Valsalva maneuver, and writhing, as this can cause re-rupture
of an unsecured aneurysm. One must also be careful to not over-sedate the patient as this
could mask the symptoms of hydrocephalus (obtundation).
• Use IV medications with short half-lives (fentanyl for example).

• Liberal use of anti-emetics is justified especially if vomiting occurs.
• Blood pressure control is enhanced with adequate analgesia.
• If anxiety is present, consider small doses of an anxiolytic such as lorazepam.
18
Blood Pressure Management: SPB <160
Avoid hypertension to prevent re-rupture
General principles:
• Current guidelines suggest treating severe hypertension in patients with an unsecured
ruptured aneurysm.
• Modest hypertension [mean arterial pressure (MAP) < 110 mmHg] may not require
treatment.
• Premorbid BPs should be considered and used to inform the risks and benefits of
treatment.
• Antihypertensive medications that are short acting, titratable, and can be administered
as a continuous infusion, such as nicardipine or clevidipine, to reduce the systolic
pressure < 160 mmHg, or the MAP < 110 mmHg, should be used, keeping in mind the
principles mentioned above.
• Nitroprusside and nitroglycerine should be avoided because these agents may cause
cerebrovascular dilation and thereby increase ICP.
See the ENLS Pharmacology protocol.
19
Decline in Neurological Exam

Worsening neurological examination?
There are several immediate causes of early (within the first hour) neurological
decompensation.
• Re-rupture of the aneurysm: repeat head CT is diagnostic
• Worsening hydrocephalus: repeat head CT is diagnostic; need for external
ventricular drain (EVD) is now paramount; give mannitol while arranging for EVD
placement
• Seizure: treat with phenytoin or levetiracetam load
• Cardiopulmonary cause: neurogenic pulmonary edema, catecholamine
cardiomyopathy manifesting with worsening hypoxia or hypotension.
Echocardiography is diagnostic of cardiomyopathy.
20
Hydrocephalus
Are the ventricles dilated?
Hydrocephalus is caused by blockage of CSF absorption and is diagnosed by interpreting the

head CT scan. If the patient is obtunded or comatose, it is important to provide ventricular
drainage by having an external ventricular drain placed. This both treats the hydrocephalus
and provides a monitor of ICP.
• If a neurosurgeon is not available at your hospital and hydrocephalus is present,

consider treating the patient with mannitol 1 gm/kg and expediting transfer to a
facility with neurosurgical capability within the next hour.
21
Consider Antifibrinolytic Agents
Preventing re-rupture
Preventing re-rupture of the aneurysm is a major goal of initial therapy.
• Antifibrinolytic agents such as aminocaproic acid and tranexamic acid can reduce
aneurysmal re-rupture. However, these agents also raise the risk of deep venous
thrombosis (DVT), pulmonary embolus (PE), and ischemic stroke if they are
continued. If the patient is free of recent myocardial infarction, DVT/PE or any known
hypercoagulable state, many centers administer antifibrinolytic agents until the
aneurysm can be secured; this may be an appropriate strategy but should be
discussed with the consultant.
22
Traumatic Brain Injury Protocol
Version 4.0
Authors
Lara L. Zimmermann, MD
Marlina E. Lovett, MD
Halinder S. Mangat, MD
Protocol developed by: Lara L. Zimmermann, MD

Traumatic Brain Injury Algorithm

Table of Contents
Traumatic Brain Injury Algorithm ...............................................................................................2
Checklist ...................................................................................................................................3
Communication .........................................................................................................................3
Traumatic Brain Injury ...............................................................................................................5
Diagnosis and Classification ..................................................................................................5
Prevention of Secondary Brain Injury ........................................................................................6
Applied throughout continuum of care of TBI .........................................................................6
Prehospital Care .......................................................................................................................7
Spinal Motion Restriction ...........................................................................................................8
ABCDE .....................................................................................................................................9
Airway....................................................................................................................................9
Breathing ...............................................................................................................................9
Circulation .............................................................................................................................9
Disability ..............................................................................................................................10
Expose/Environment............................................................................................................11
Obtain History .........................................................................................................................12
The Essential Neuro Exam in Trauma .....................................................................................13
Avoid Prophylactic Hyperventilation ........................................................................................15
Treatment of Suspected Brain Herniation in the Prehospital Setting........................................16
EMERGENCY DEPARTMENT CARE .....................................................................................17
Continue Priorities of Prehospital Care ................................................................................17
Resuscitation & Stabilization ...................................................................................................18
Post-Resuscitation GCS and Pupillary Exam ..........................................................................19
Obtain Head CT ......................................................................................................................20
Neurosurgery Consultation ......................................................................................................21
Indications for ICP monitoring ..............................................................................................21
Avoid Hypoxemia and Hypotension .........................................................................................23
Treat Brain Herniation & Increased ICP ..................................................................................24
Correct Coagulopathy .............................................................................................................25
Recognition and treatment ...................................................................................................25
Seizure Prophylaxis ................................................................................................................26
Analgesia & Sedation ..............................................................................................................27
Avoid Prophylactic Hyperventilation, Steroids, Hypothermia ...................................................28
Prophylactic Hyperventilation is not recommended. .............................................................28
Steroids Contraindicated .....................................................................................................28
Hypothermia ........................................................................................................................28
Inter or Intra-hospital Transfer .................................................................................................29
ICU Admission ........................................................................................................................30
Follow Institutional Severe TBI Management Protocol ............................................................31
Neurocritical Care Consultation ...............................................................................................32
2
Checklist
☐ Secure airway and maintain normal ventilation (PaCO2 35–45)
☐ Hemodynamic stabilization: maintain ≥ 110 mmHg for patients 15–49 or > 70 years;
maintain SBP ≥ 100 mmHg for patients 50–69 years
☐ Maintain SpO2 > 90%
☐ Restrict motion of C-spine
☐ Determine post-resuscitation GCS score; pupil size, symmetry, and light reactivity
☐ Treat brain herniation and increased ICP
☐ Obtain CT head and C-spine
☐ Neurosurgical consultation
☐ Correct coagulopathy
☐ Seizure prophylaxis
☐ Repeat GCS and pupillary examination hourly
☐ Coordinate safe inter- or intra-hospital transfer
Communication
☐ Age
☐ Sex
☐ Pre-injury health, including home medications (antiplatelet or anticoagulation)
☐ Mechanism and time of injury
☐ Loss of consciousness, seizure, post-traumatic amnesia, helmeted?
☐ Post-resuscitation GCS and pupil size shape and reactivity
☐ Head CT findings
☐ State of C-spine: cleared, not cleared, injury
☐ Other injuries
☐ Current vital signs
☐ Current ventilation therapy including EtCO2 and most recent ABG
☐ Labs: Coagulation parameters, CBC, sodium, BUN, Cr, alcohol level, UTOX
☐ Treatments provided (reversal of anticoagulation, blood transfusions, seizure prophylaxis,
etc.)
☐ Neurosurgical plan for surgery, ICP monitoring or not
3
Sample sign-off narrative

“Hello there–I am signing out a 42-year-old man who presented tonight after a high-speed
motorcycle accident that occurred about 11 p.m.”
“The patient was driving and lost control and was found on the road about 20 feet from his
motorcycle”
“The accident was witnessed; there was positive loss of consciousness and he had one
convulsive seizure lasting about 1 min witnessed by EMS”
“He was wearing a helmet”
“Initial GCS on the scene was 4. Post-resuscitation GCS here in the ED is 7 (E1, M4, V2). He
was withdrawing symmetrically and moaning before intubation. Pupils are about 3 mm and
briskly reactive”
“Head CT shows a 4 mm acute left SDH and bifrontal hemorrhagic contusions. CT C-spine
was negative for fracture, but C-spine is not cleared”
“No other injuries were identified on his primary or secondary trauma survey”
“He is intubated and hemodynamically stable; SBP 120 mmHg and SpO2 96% on F02 60%
and PEEP 8. EtCO2 35 mmHg”
“Labs coags were normal, Na 140 and platelets 240”
“He has received levetiracetam 1 g IV × 1, 1L normal saline and no blood products”
“Neurosurgery has been consulted and plans to place an external ventricular drain as soon as
he gets to the ICU”
“He will be transferred to the Neurotrauma ICU, bed 4”
4
Traumatic Brain Injury

Diagnosis and Classification
Traumatic brain injury (TBI) is defined as an alteration in brain function or other evidence of
brain pathology caused by an external force. The diagnosis of TBI is based on identifying a
traumatic mechanism and/or physical signs of trauma to the brain in a patient with neurological
signs or symptoms. The Glasgow Coma Scale (GCS) score ideally should be determined in
the prehospital setting and repeated upon arrival to the ED and following resuscitation. The
severity of the injury is classified by the post-resuscitation GCS score and graded as mild,
moderate, or severe.
• Mild TBI: GCS 13-15
• Moderate TBI: GCS 9-12
• Severe TBI: GCS 3-8
The GCS score will be affected by hypotension, hypoxemia, sedation, and paralysis.
Therefore, ideally it should be recorded in the ED following resuscitation and prior to
administration of sedation or pharmacological paralysis. Scoring of the GCS should be broken
down by categories for eye, motor and verbal responses in addition to the total of all values
(example: GCS 10 (E3, V3, M4)). The best observed score should be recorded. For example,
if a patient follows commands with the right upper extremity but only withdraws with the left
upper extremity, then a GCS motor score of 6 (not 4) should be awarded.
Score (3-
Examination Response 15)
Eye Opening Response (E) Eyes open spontaneously 4
Eyes open to speech 3
Eyes open to pain 2
Eyes do not open 1
Motor Response (M) Follows commands 6
Localizes (purposeful) movement toward a painful stimulus 5
Withdraws (normal flexion) from pain 4
Abnormal flexion to pain (decorticate) 3
Extension response to pain (decerebrate) 2
None 1
Verbal Response (V) Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
5
Prevention of Secondary Brain Injury
Applied throughout continuum of care of TBI
The primary brain injury following TBI occurs at the time of impact and results in altered level
of consciousness. With increasing severity of TBI, there is a risk of multicompartmental
hemorrhagic injury, including acute subdural hematoma (SDH), epidural hematoma (EDH),
cerebral contusion, traumatic subarachnoid hemorrhage (tSAH), diffuse axonal injury (DAI)
and cerebral edema with brain compression and shift. Individuals who survive their initial
trauma remain at high risk for secondary brain injury from hypoxia, ischemia, hypotension,
hematoma expansion, cerebral edema, brain compression, intracranial hypertension, seizures,
and fever. The role of health care providers is to anticipate secondary brain injury, detect it
early and treat it quickly in order to prevent neurological worsening.
6
Prehospital Care
Fifty percent of all deaths from TBI occur within the first few hours of injury. Prehospital care of
TBI patients by trained paramedical personnel is critical to prevent secondary brain injury and
optimize neurological outcomes for children and adults. Prehospital providers must obtain a
relevant history, provide best resuscitative care including maintaining a patent airway, achieve
appropriate oxygenation, ventilation and circulation, ensure spinal motion restriction and
provide safe and expedient transport to the most proximate and appropriate trauma center.
Priorities in the prehospital setting include:

▪ Spinal motion restriction
▪ ABCs: Maintain SpO2 > 90%, SBP > 100 – 110 mmHg
▪ Obtain relevant history: mechanism of injury, medications, loss of consciousness, post-
traumatic amnesia, post-traumatic seizures
▪ Determine GCS, pupillary examination
▪ Avoid prophylactic hyperventilation (maintain ETCO2 35-40 mmHg)
▪ Treat brain herniation
7
Spinal Motion Restriction

Following suspected trauma, a cervical collar and spinal motion restriction is advised to
prevent iatrogenic spinal cord injury until spinal stability is established.
Advanced Trauma Life Support (ATLS) protocols should be followed and head computed
tomography (CT) obtained expeditiously after the primary survey is complete and the patient is
hemodynamically stable. Cervical spine CT imaging is indicated in the setting of moderate-
severe TBI because C-spine injuries occur in up to 10% of patients with blunt TBI. A negative
C-spine CT may not be sufficient to rule out ligamentous injuries and the C-spine should
remain immobilized until it can be cleared.
Please refer to the ENLS Protocol Traumatic Spine Injury for a more detailed discussion of
spinal precautions and clearance.
8
ABCDE
The ENLS TBI algorithm is designed to emphasize the importance of preventing secondary
brain injury across the continuum of care from the time of initial trauma through admission to
the ICU.
Airway
It is imperative to maintain oxygen saturation > 90%. Hypoxia, defined as O2 saturation < 90%
or a PaO2 < 60mmHg, even for a brief period of time, is associated with increased mortality
following a TBI. The combination of prehospital hypotension and hypoxia are associated with
twice the risk of death than hypotension or hypoxia alone.
▪ Maintain SpO2 > 90%
Breathing
Normal ventilation targeting a constant end-tidal CO2 (ETCO2) 35-40 mmHg should be
provided. If ETCO2 is not available an adult patient should receive assisted ventilation at a rate
of 10 breaths/minute.
▪ Maintain normal ventilation, ETCO2 35-40 mmHg
Prophylactic hyperventilation should be avoided unless there are signs of brain herniation.
▪ If signs of herniation, then mild hyperventilation (ETCO2 30-35 or RR= 20

breaths/minute in an adult) is indicated
Circulation
Hypotension results in brain hypoperfusion, secondary brain injury and increased mortality.
The combination of prehospital hypotension and hypoxia are associated with twice the risk of
death than hypotension or hypoxia alone.
▪ Goal SBP ≥ 100 – 110 mmHg for adults

o SBP ≥ 110 mmHg for patients 15-49 or > 70 years
o SBP ≥ 100 mmHg for patients 50 – 69 years old.
▪ For children, SBP should be maintained at least > 5th percentile for age (70 mmHg +
(age x 2)).
9
Disability
The severity of traumatic brain injury is classified by the post-resuscitation Glasgow Coma
Scale (GCS) score and graded as mild, moderate, or severe. The GCS score ideally should be
determined in the prehospital setting and repeated upon arrival to the ED and following
resuscitation.
Score (3-
Eyes open to pain 2
Eyes do not open 1
None 1
Confused 4
None 1
administration of sedation or pharmacological paralysis. Scoring of the GCS should be broken
down by categories for eye, motor and verbal responses in addition to the total of all values
(example: GCS 10 (E3, V3, M4)). The best observed score should be recorded. For example,
if a patient follows commands with the right upper extremity but only withdraws with the left
upper extremity, then a GCS motor score of 6 (not 4) should be awarded.
10
Expose/Environment
Prehospital providers can provide valuable information about the trauma scene and body
presentation when arriving at the emergency center. A systematic way to receive report is
helpful to account for these details, and severity of other injuries when caring for the TBI
patient. During primary assessment the patient must be fully exposed, yet not left exposed to
avoid development of hypothermia.
11
Obtain History
In the prehospital and emergency department setting, pertinent history includes:
- The mechanism of injury

- Presence / absences of head strike
- Helmet use
- Loss of consciousness and duration
- Post-traumatic amnesia
- Occurrence of early post-traumatic seizures
- Medications (particularly anti-platelet or anticoagulant drugs)
- Alcohol or drug use
This information can be used to activate appropriate trauma protocols and direct subsequent
care.
12
The Essential Neuro Exam in Trauma

Traumatic brain injury severity and classification is based on the post-resuscitation Glasgow
Coma Scale (GCS) score and graded as mild, moderate, or severe.
Score (3-
Eyes open to pain 2
Eyes do not open 1
None 1
Confused 4
None 1
The GCS score ideally should be determined in the prehospital setting and repeated upon
arrival to the ED and following resuscitation. The GCS score will be affected by hypotension,
hypoxemia, sedation, and paralysis. Therefore, ideally it should be recorded in the ED
following resuscitation and prior to administration of sedation or pharmacological paralysis.
Scoring of the GCS should be broken down by categories for eye, motor and verbal responses
in addition to the total of all values (example: GCS 10 (E3, V3, M4)). The best observed score
should be recorded. For example, if a patient follows commands with the right upper extremity
but only withdraws with the left upper extremity, then a GCS motor score of 6 (not 4) should be
awarded.
Pupillary size, shape, and reactivity to light should be tested. These are critical pieces of
information for early neurosurgical decision-making. Pupillary asymmetry, defined as a
difference greater than 1mm, should be immediately recognized because it may indicate
ongoing brain herniation and imminent death if not treated.
13
The GCS score and pupillary examination should be recorded frequently during prehospital
and ED care as well as in the ICU to identify neurological worsening or improvement over time.
Recognizing a decline in the GCS score ≥2 is crucial because it may indicate secondary brain
injury from hematoma expansion, increasing cerebral edema, brain shift/herniation or seizures.
14
Avoid Prophylactic Hyperventilation

Primary TBI occurs at the time of impact. Prevention of secondary brain injury is the focus of
TBI management from initial trauma through the prehospital setting, emergency department
(ED), and intensive care unit (ICU) admission.
It is important to avoid prophylactic hyperventilation in the first 24 hours following injury unless
there are signs of brain herniation such as a dilated or non-reactive pupil, Cushing reflex
(hypertension plus bradycardia) or extensor/decerebrate posturing because early prophylactic
hyperventilation is associated with increased mortality. Hyperventilation, particularly within the
first 24 hours after head trauma, will decrease cerebral blood flow (CBF) when the brain is
hyperglycolytic and may result in cerebral ischemia.
Patients with moderate-severe TBI should be re-assessed frequently for clinical signs of
intracranial hypertension or brain herniation including asymmetric, dilated or non-reactive
pupils, motor exam with extensor posturing, Cushing reflex (hypertension plus bradycardia) or
decline in GCS of more than 2 points. If these signs are present, then hyperventilation (ETCO2
30-35 or respiratory rate of 20 breaths/minute in an adult) may be used as a temporizing
measure until definitive treatment can occur.
15
Treatment of Suspected Brain Herniation in the Prehospital

Setting
Prehospital care of TBI patients by trained paramedical personnel is critical to prevent
secondary brain injury and optimize neurological outcomes for children and adults with TBI.
The severity of injury is assessed using the Glasgow Coma Scale (GCS) score and classified
by GCS of 13-15 as mild TBI, 9-12 as moderate TBI, and 3-8 as severe TBI. Patients with
moderate-severe TBI should be assessed frequently for clinical signs of intracranial
hypertension or brain herniation including asymmetric, dilated or non-reactive pupils, motor
exam with extensor posturing, Cushing reflex (hypertension plus bradycardia) or decline in
GCS of more than 2 points. If these signs of brain herniation are present, then mild
hyperventilation (ETCO2 30-35 or respiratory rate of 20 breaths/minute in an adult) may be
used as a temporizing measure in attempt to reverse the herniation en route to an emergency
department.
16
EMERGENCY DEPARTMENT CARE
Continue Priorities of Prehospital Care
Upon arrival to the emergency department (ED) the major priorities from the field should be
maintained including spinal motion restriction, avoiding prophylactic hypoventilation, continuing
resuscitation and stabilization, determining post-resuscitation GCS and pupillary examination,
and treating brain herniation.
17
Resuscitation & Stabilization

Trauma victims should be assessed, resuscitated and stabilized per the Advanced Trauma Life
Support (ATLS), Advanced Cardiac Life Support (ACLS) and Pediatric Advanced Life Support
(PALS) protocols.
The priorities of resuscitation care include:

▪ Hemorrhage control: assessment and stabilization of circulation
▪ ABCs
▪ Obtain IV / IO access
▪ FAST assessment for internal bleeding
▪ Maintain SpO2 > 90%, SBP ≥ 100 – 110 mmHg, PaCO2 35-40 mmHg
▪ Avoid hypotension/hypotensive resuscitation in the setting of TBI
▪ If post-resuscitation GCS score ≤ 8 → rapid sequence intubation and activate
institutional severe TBI protocol.
18
Post-Resuscitation GCS and Pupillary Exam

TBI severity (mild, moderate or severe) is defined by the post-resuscitation Glasgow Coma
Scale (GCS) score.
Score (3-
Eyes open to pain 2
Eyes do not open 1
None 1
Confused 4
None 1
administration of sedation or pharmacological paralysis. The best observed score should be
recorded. For example, if a patient follows commands with the right upper extremity but only
withdraws with the left upper extremity, then a GCS motor score of 6 (not 4) should be
awarded.
The size and shape of pupils, and their reactivity to light, should also be tested. Pupillary
asymmetry, defined as a difference greater than 1mm, should be immediately recognized
because it may indicate ongoing brain herniation and imminent death if not treated.
19
Obtain Head CT
In the emergency department, Advanced Trauma Life Support (ATLS) protocols should be
followed first and head computed tomography (CT) obtained expeditiously after the primary
survey is complete and the patient is hemodynamically stable.
Head computed tomography (CT) is the recommended neuroimaging test in trauma due to fast
image acquisition and reliable detection of acute blood. The primary purpose of the initial head
CT is to identify any intracranial hemorrhage that requires emergent neurosurgical intervention.
Acute TBI often results in a multicompartmental intracranial hemorrhagic injury. An acute SDH
appears as a homogenous hyperdense concave or crescent-shaped mass that crosses suture
lines. An acute EDH is characteristically lentiform and does not cross cranial suture lines.
Hemorrhagic cerebral contusions are typically seen in the frontal or anterior temporal lobes
can have a “salt and pepper” appearance with mixed density acute blood. Intracranial air
suggests an open skull fracture, craniofacial trauma or injury to a sinus. The location and size
of the brain hemorrhage(s) should be determined as well as an estimate of the degree of mass
effect, cerebral edema and brain shift by measuring the amount of midline shift of the third
ventricle and evaluating if the perimesencephalic cisterns are patent, partially compressed or
absent. The cranial vault and facial bones should be reviewed for fractures or penetrating
objects.
General indications for neurosurgical intervention, including trauma craniotomy and/or

hematoma evacuation, are described in the Neurosurgical Consultation section.
20
Neurosurgery Consultation
Neurosurgery should be consulted for all patients with known or suspected head trauma with
abnormal neuroimaging or level of consciousness. If neurosurgical expertise is not available,
every effort must be made to transfer a patient with moderate-severe TBI to an appropriate
facility where such expertise is available. Adherence to the Brain Trauma Foundation
Guidelines, which are based on a systematic evidence-based approach, improves neurological
outcomes in both children and adults.
Indications for ICP monitoring

• Intracranial pressure (ICP) monitoring is indicated in patients with GCS score ≤ 8 and
an abnormal head CT.
• Elevated ICP should also be suspected and ICP monitoring considered in the setting of
an apparently “normal” head CT if the GCS score ≤ 8 with two or more of the following
present:
o Age > 40 years
o Motor posturing
o Systolic blood pressure (SBP) < 90mmHg
General indications for neurosurgical intervention including trauma craniotomy and/or

hematoma evacuation include [28-32]:
▪ Acute SDH: > 10mm thickness or > 5mm midline shift; patients with an acute SDH of
any size who experience a decline in GCS ≥ 2 points or have asymmetric or non-
reactive pupils
▪ Acute EDH: > 30cm3, > 15mm thickness, or > 5mm midline shift or GCS ≤ 8
▪ Cerebral contusions: comatose patients with survivable injuries and brain hemorrhage
resulting in midline shift > 5mm or herniation
▪ Cerebellar hemorrhage resulting in mass effect, brainstem compression or
hydrocephalus
▪ Depressed skull fracture: open fractures depressed greater than the thickness of the
cranium
Neurosurgical consultation is also recommended for patients with the following injuries to
determine if neurosurgical management is indicated:
▪ Skull fracture
▪ Signs of CSF leak with clear or serosanguinous fluid from ears or nares
▪ Lateralizing signs on neurological examination (i.e., unequal pupils, focal weakness)
▪ Cerebrovascular injury (refer to ENLS Acute Ischemic Stroke module)
▪ C-spine injury (refer to ENLS Traumatic Spine Injury module)
21
When consulting neurosurgery, it is important to communicate the following key
information:
- Age (estimated if unknown)

- Mechanism and time of injury (if known)
- Prehospital and post-resuscitative GCS scores including best eye opening, verbal and
motor components.
- Pupillary size, shape, symmetry and reactivity to light
- Head CT and C-spine results
- History of anticoagulant or antiplatelet medications and any treatments provided
22
Avoid Hypoxemia and Hypotension

The ENLS TBI algorithm is designed to emphasize the importance of preventing secondary
brain injury across the continuum of care from the time of initial trauma through admission to
the ICU.
Post-injury hypoxia and hypotension result in secondary brain injury and must therefore be
prevented.
Hypoxia, defined as O2 saturation < 90% or a PaO2 < 60mmHg, even for a brief period of time,
is associated with increased mortality following a TBI. Hypotension results in brain
hypoperfusion, secondary brain injury and increased mortality. The combination of prehospital
hypotension and hypoxia are associated with twice the risk of death than hypotension or
hypoxia alone.
▪ Maintain SpO2 > 90%

▪ Maintain SBP ≥ 100 – 110 mmHg for adults
o SBP ≥ 110 mmHg for patients 15-49 or > 70 years
o SBP ≥ 100 mmHg for patients 50 – 69 years old.
▪ For children, SBP should be maintained at least > 5th percentile for age (70 mmHg +
(age x 2)).
23
Treat Brain Herniation & Increased ICP

Signs of intracranial hypertension or brain herniation include:
• Dilated and nonreactive pupils
• Asymmetric pupils
• Motor exam that demonstrates extensor posturing
• Progressive decline in neurologic condition (decrease in GCS > 2 points) that are not
associated with non-TBI causes
• Cushing reflex (hypertension, bradycardia, irregular respirations)
If signs of intracranial hypertension or herniation are present, the patient should be treated
presumptively for high ICP while simultaneously facilitating the placement of an ICP monitor.
Treatment of intracranial hypertension or brain herniation include medical therapies and
surgical therapies.
Intracranial hypertension or “high ICP” cannot reliably be diagnosed by clinical examination or

brain imaging alone. While head CT findings indicate mass effect and may suggest high ICP, a
reliable relationship does not exist between the admission CT and subsequent development of
high ICP in patients with severe TBI. Because intracranial hypertension leads to secondary
brain injury, management of severe TBI patients using information from ICP monitoring is
recommended to reduce in-hospital mortality and 2-week post-injury mortality.
Medical management of elevated ICP (ICP > 22 mmHg sustained) includes:

• Elevate HOB 30 degrees
• Drain CSF (if available)
• Hyperosmolar therapy
o IV bolus with mannitol
o IV bolus hypertonic saline
• Optimize cerebral perfusion (SBP > 100-110 and CPP 60-70mmHg) in adults
• Mild hyperventilation
• Optimize analgesia and sedation (see ENLS: Pharmacotherapy)
• Maintain normothermia
• Start continuous EEG monitoring and treat seizures
Please refer to ENLS: Intracranial Hypertension and Herniation module for detailed
discussion of treatment of high ICP.
Please refer to ENLS: Pharmacotherapy module for a detailed discussion of hyperosmolar

therapies, analgesia and sedation, antiseizure medications.
24
Correct Coagulopathy
Recognition and treatment
The incidence of coagulopathy in TBI is high. Coagulopathy associated with trauma has
several possible mechanisms, but in TBI, the principal process involves tissue factor release.
Studies of TXA in TBI for hemostasis in TBI are ongoing. A pharmacological cause of
coagulopathy due to antiplatelet or anticoagulant medications, such as warfarin or direct oral
anticoagulants is also common
Routine laboratory measures are indicated:

▪ PT/PTT/INR
▪ Platelet count
▪ Finbrinogen
▪ Thromboelastography (TEG) if available
▪ Factor Xa levels if DOAC suspected
Expeditious detection and correction of systemic coagulopathy in the first hour after TBI is
indicated to reduce the risk of intracranial hematoma expansion and associated secondary
brain injury.
See ENLS: Pharmacotherapy for detailed antidotes and dosing.
25
Seizure Prophylaxis
Posttraumatic seizures are a common complication of moderate-severe TBI and are classified
as:
▪ Immediate seizure (within 24 hours of injury)
▪ Early seizure (24 hours - 7 days after injury)
▪ Late seizure (> 7 days after injury).
The use of prophylactic antiseizure medication is recommended for 7 days following TBI to
decrease the incidence of early posttraumatic seizures.
Two commonly used antiseizure medications in the setting of moderate-severe TBI are:
▪ Phenytoin
▪ Levetiracetam
26
Analgesia & Sedation

Children and adults with severe TBI (GCS ≤ 8) require tracheal intubation for airway protection.
Intravenous analgesia and sedation are often needed to ensure pain and agitation are
adequately controlled and physiological targets for goal directed TBI care are met. In choosing
sedative medications, short acting agents with minimal hemodynamic effects are preferred to
allow hourly neurological examinations and rapid detection of any neurological worsening.
See the ENLS: Airway, Ventilation and Sedation for a more detailed discussion of Analgesia
& Sedations strategies.
27
Avoid Prophylactic Hyperventilation, Steroids, Hypothermia
Prophylactic Hyperventilation is not recommended.
Primary TBI occurs at the time of impact. Prevention of secondary brain injury is the focus of
TBI management from initial trauma through the prehospital setting, emergency department
(ED), and intensive care unit (ICU) admission.
It is important to avoid prophylactic hyperventilation in the first 24 hours following injury

unless there are signs of brain herniation such as a dilated or non-reactive pupil, Cushing
reflex (hypertension plus bradycardia) or extensor/decerebrate posturing because early
prophylactic hyperventilation is associated with increased mortality. Hyperventilation,
particularly within the first 24 hours after head trauma, will decrease cerebral blood flow (CBF)
when the brain is hyperglycolytic and may result in cerebral ischemia.
Patients with moderate-severe TBI should be re-assessed frequently for clinical signs of
intracranial hypertension or brain herniation including asymmetric, dilated or non-reactive
pupils, motor exam with extensor posturing, Cushing reflex (hypertension plus bradycardia) or
decline in GCS of more than 2 points. If these signs are present, then hyperventilation
(ETCO2 30-35 or respiratory rate of 20 breaths/minute in an adult) may be used as a
temporizing measure until definitive treatment can occur.
Steroids Contraindicated
Administration of steroids is harmful and increases the risk of death in patients with severe
TBI.
Hypothermia
Currently, the literature suggests that there is no benefit to early prophylactic hypothermia or
therapeutic hypothermia for intracranial hypertension to improve neurological outcomes in TBI.
However, targeted temperature management for prevention of fever is appropriate.
28
Inter or Intra-hospital Transfer

Patients with moderate-severe TBI should be transferred to a trauma center with neurosurgical
capabilities, including the availability of pediatric neurosurgeons for pediatric patients.
It is important that the following key elements are communicated between the transferring and
accepting physician. Click here to view the TBI Communication Checklist (link).
In the first critical hours following TBI, both inter- and intra-hospital transport for diagnostic or
therapeutic procedures regularly occurs. The priority during transport of a patient with TBI is to
prevent secondary brain injury by maintaining minute ventilation for a stable PaCO 2 and
through prompt treatment of hypotension, oxygen desaturation, increased ICP or seizures that
may occur. The checklist for safe transport of patients with moderate-severe TBI,
including pre-transport assessment, transport and post-transport evaluation is shown
here (link).
29
ICU Admission
Patients with mild, moderate, and severe TBI remain at risk for neurological decline in the first
24 hours after injury due secondary brain injury from a variety of causes including progressive
cerebral edema and expansion of intracranial hematomas. Hemorrhagic expansion of
traumatic cerebral contusions occurs in about 50% of cases. Patients with moderate-severe
TBI should be admitted to an intensive care unit (ICU) with trauma, neurosurgery and
neurocritical care expertise and monitored with hourly neurological examinations with special
focus on GCS and pupillary examination in order to rapidly detect neurological worsening
which occurs about 25% of the time. Recognizing a decline in the GCS score ≥ 2 is crucial
because it may indicate secondary brain injury from hematoma expansion, increasing cerebral
edema, brain shift/herniation or seizures. A repeat head CT should be strongly considered at 6
hours following initial injury to evaluate for stable or worsening intracranial hemorrhage
30
Follow Institutional Severe TBI Management Protocol
A systematic, evidence-based approach to management of TBI is recommended including
adherence to institutional TBI protocols at trauma centers that follow the Brain Trauma
Foundation Guidelines. A trauma patient with a post-resuscitation GCS score ≤ 8 should
necessitate activation of the institutional severe TBI protocol.
A systematic evidenced-based approach to the management of pediatric TBI is equally

important for children as it is for adults. The PEGASUS study assessed physician adherence
to three key performance indicators [early initiation of enteral nutrition, avoidance of
hypocarbia (PaCO2 < 30mmHg) and adequate cerebral perfusion (CPP > 40mmHg) for 72
hours after severe TBI] and found that adherence to these performance indicators resulted in
improved survival and a more favorable discharge disposition for children.
31
Neurocritical Care Consultation

Neurocritical care is a unique subspecialty focusing on the optimal management of children
and adults with life threating brain injuries, including traumatic brain injury (TBI). Patients with
moderate-severe TBI (and in some cases mild TBI when there is intracranial hemorrhage)
should be admitted to an intensive care unit (ICU) with trauma, neurosurgery and neurocritical
care expertise and monitored with hourly neurological examinations.
32
Traumatic Spinal Cord Injury Protocol
Version 4.0
Authors
Jeff W. Chen, MD, PhD
Neha S. Dangayach, MD
Kerri L. LaRovere, MD

Traumatic Spinal Cord Injury Algorithm

Checklist
□ Spinal motion restriction with cervical collar, and maintain spine precautions with “flat/bed
rest” until seen by spine specialist
□ Keep SBP > 90 mmHg with IV fluids and vasoactive medications as needed
□ Administer supplemental O2 if SpO2 < 92%
□ Consider early intubation for failure of ventilation per Table 1
□ Rule out other causes of hypotension such as hemorrhage, pneumothorax, cardiac
dysfunction
Do not assume neurogenic shock
Communication
□ Age
□ Mechanism of injury
□ Vital signs
□ Basic neurologic examination including any sensory deficit, motor deficit, “level” of deficit,
and rectal tone and sensation
□ Additional traumatic injuries
□ Interventions and medications administered including IV fluids and blood products
administered and any vasoactive infusions with dose
□ CT scan including location of fractures, displacement of fragments, dislocation and/or MRI
scan including spinal cord signal change and ligamentous injury noted
3
Traumatic Spine Injury

Cervical spine injury
Traumatic Spine Injury (TSI): This topic covers TSI as it relates to the cervical spine. Many of
the concepts apply to less common thoracic or lumbar spine trauma. One should suspect
cervical spine injury when there is:
• A worrisome mechanism
• Midline cervical spine tenderness
• Neurological findings consistent with acute spinal cord injury
Initial management should include:

• Airway
• Breathing
• Circulation
• Immobilization
• Detailed examination
• Imaging, if necessary
• Treatment
Notes:
• You may put the patient in reverse Trendelenburg if at risk for aspiration.
• Backboards should be used for transport only because of the risk of skin breakdown.
Thoracic and lumbar immobilization can be accomplished in an ED stretcher or
hospital bed.
4
Assess Airway
Who to intubate
Patients with TSI can be at exceptionally high risk of loss of airway due to a combination of:
• Airway edema
• Loss of diaphragmatic innervation (C3, C4, and C5 innervate the diaphragm)
• Failure to ventilate
• Loss of chest and abdominal wall strength
All patients with a complete cervical TSI C1-C4 should be considered for early, elective
intubation and mechanical ventilation.
Patients with incomplete or lower injuries will have a high degree of variability in their ability to
maintain adequate oxygenation and ventilation. General parameters for urgent intubation:
• Complaint of "shortness of breath", inability to "catch my breath", or breathlessness
• Vital Capacity < 10 ml/kg or decreasing vital capacity
• Appearance of "quad breathing" (abdomen goes out sharply with inspiration). When
in doubt, it is better to intubate a patient with a cervical TSI electively rather than wait
until it needs to be done emergently. Patients will typically develop worsening of
their primary injury shortly after admission due to cord edema and progressive loss
of muscle strength. Patients with very high (above C3) complete TSI will almost
invariably suffer a respiratory arrest in the field and, if not intubated by prehospital
providers, typically present in cardiac arrest.
How to intubate
Generally, patients with cervical TSI who require intubation should be intubated using an
awake, fiberoptic approach by an experienced provider. Video laryngoscopy can be a
reasonable alternative to fiberoptic intubations, especially in emergent scenarios, or if
fiberoptic equipment is not available. Patients who require urgent or emergent intubation,
should be intubated using rapid sequence intubation (see ENLS protocol Airway, Ventilation
and Sedation).
Special issues related to intubation in TSI:

• Aspiration precaution should always be taken as for any emergent intubation.
• Cervical in-line stabilization must be carefully maintained throughout all intubation
attempts.
• No particular RSI regimen is preferred, but these patients will already have loss of
vasomotor tone and therefore medications that diminish the catecholamine surge
may result in hypotension and bradycardia.
5
Breathing
Patients with TSI are at high risk of inadequate oxygenation and ventilation. This is due to a
combination of factors:
• Loss of diaphragmatic function
• Loss of ability to cough and deep breathe due to loss of chest wall and abdominal
musculature function
• Aspiration
• Retention of secretions
• Atelectasis
• Concomitant injuries (pulmonary contusions, pneumothorax, rib fractures)
• Supplemental oxygen should be supplied to all patients with cervical TSI if
necessary. Hypoxia is extremely detrimental to patients with neurological injury.
Noninvasive methods of ventilation should be used with caution as the inability to
cough and clear secretions may lead to an increased risk of aspiration.
6
Circulation
Patients with TSI (above T6) often develop neurogenic shock. The patient suffers a
"sympathectomy" resulting in unopposed vagal tone. This leads to a distributive shock with
hypotension and bradycardia.
• Patients are generally hypotensive with warm, dry skin. This is due to the loss of
sympathetic tone resulting in an inability to redirect blood flow from the periphery to
the core circulation.
• Bradycardia is a characteristic finding of neurogenic shock and can help to
differentiate from other forms of shock.
Care should be taken not to "assume" that a patient has neurogenic shock due to a lack of
tachycardia, as young healthy people and patients on premorbid beta-blockers, etc. will often
not manifest tachycardia in the setting of hemorrhage.
• As a general rule, the higher and more complete the injury, the more severe and
refractory the neurogenic shock.
• These signs can be expected to last from one to three weeks.
• Patients may develop manifestations of neurogenic shock hours to days following
injury due to progressive edema and ischemia of the spinal cord resulting in
"ascension" of their injury.
• In the patient with traumatic injury, other sources of hypotension (hemorrhage, TBI)
MUST be sought and ruled out.
o Pitfall: "Spinal shock" has nothing to do with hemodynamics, but rather refers to
the loss of deep tendon stretch reflexes because of the spinal injury.
Management of hypotension: maintain MAP 85-90 mm Hg for the first 7 days
First line treatment of neurogenic shock is always fluid resuscitation to maintain euvolemia.
• The loss of sympathetic tone leads to vasodilation and the need for an increase in
the circulating blood volume ("filling the tank")
• Second line therapy includes vasopressors and/or inotropes.
• Norepinephrine - has both alpha and some beta activity thereby improving both
blood pressure and bradycardia. Norepinephrine is the preferred agent.
• Phenylephrine - pure alpha agonist. Phenylephrine is commonly used and easily
titrated. Lacks beta activity so does not treat bradycardia and may actually worsen it
through reflexive mechanisms.
• Dopamine - need high doses (> 10 mcg/kg/min) for alpha effect, but does have
significant beta effects at lower doses. May lead to inadvertent diuresis at lower
doses exacerbating relative hypovolemia.
• Epinephrine - an alpha and beta agonist. Epinephrine causes vasoconstriction and
increased cardiac output. High doses are often required leading to inadvertent
mucosal ischemia. Rarely used or needed.
• Dobutamine - beta agonist (inotrope) that can be useful when the loss of
sympathetic tone causes cardiac dysfunction. Caution should be used in patients
who are not adequately volume loaded as may cause hypotension.
7
The American Association of Neurological Surgeons and the Congress of Neurological
Surgeons' Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries
recommend as an option, "Maintenance of mean arterial blood pressure at 85 - 90 mmHg for
the first seven days following acute TSI to improve spinal cord perfusion." This
recommendation should be carefully weighed in patients with concomitant injuries, and the
potential risks of fluid overload and/or pressors. Institutional collaboration is recommended to
develop best practice.
8
Clinical Clearance
Can the spine be cleared clinically?
Depending on the patient's level of consciousness, one may be able to clear the patient’s
cervical spine clinically, if the patient has had either a negative CT scan, or did not meet
NEXUS or Canadian Decision Rules criteria that recommend CT imaging.
• If the patient has a normal neurologic exam, and is alert and without pain, the
cervical spine can be clinically cleared. This is done by removing the cervical collar
and having the patient rotate their head 45 degrees to each side. If they are able to
do this without significant pain, the C-Spine can be cleared. If there is significant
pain or the patient cannot perform the entire movement, replace the cervical collar.
• If the patient has altered mental status that is expected to be transient (e.g. alcohol
or drug intoxication), maintain cervical spine immobilization until reliable examination
is possible (NEXUS or Canadian C-Spine Rules) and proceed through this algorithm
from the beginning.
Who Should Be Imaged - How to "clear the cervical spine"
Point tenderness over a spinous process may indicate instability of the respective vertebral
bone. Examine the entire spine by palpation or percussion; focal spine injury often produces
highly focal tenderness.
• If focal tenderness is present, the patient may need a CT of the spine
There are two recommended systems that help you determine who you can "clinically
clear" from significant spine injury without imaging, and for whom you should perform CT/
MRI to detect fractures or spine misalignment. These are the NEXUS and Canadian Rules.
Unable to clear spine clinically: there may be ligamentous injury
If the action of self-imposed neck rotation 45 degrees to either side proves too painful to
complete, ligamentous injury is a possibility. The cervical collar should be left in place and
advanced imaging pursued (See section on Imaging). MRI may be of value to investigate
ligamentous injury if the patient cannot be clinically cleared within the first few days of injury.
9
Clearing the C-Spine - Decision Rules
Canadian and NEXUS rules
CT of the spine should be performed if any of the following are present:
Significant associated injuries:

• Multiple trauma patient needs CT of head, chest, or abdomen/pelvis
• Intubated
• Depressed level of consciousness
• Neurological deficit referable to the spine, or complaints of bilateral paresthesias
• Strong clinical suspicion of any spinal fracture
• Multiple fractures
• Pelvis fracture
• Significant head or facial trauma
CT of the spine should be considered for significant mechanism of injury:

• Motor vehicle collision with speed exceeding 35 mph
• Ejection from vehicle
• Pedestrian, bicyclist, or motorcyclist struck and thrown
• Axial load injury (vehicle roll-over or diving injury)
• Fall in excess of 10 ft.
• Death at accident scene
Patient Factors
• Age > 65 years
• DJD, ankylosing spondylitis, rheumatoid arthritis
• Depressed level of consciousness
• Known cervical spine injury
• History of prior spine surgery
If the mechanism is worrisome (clear history of neck injury or circumstances that have a
reasonable likelihood of causing spinal trauma) one can consider using two validated clinical
scales. These are the NEXUS Rules and the Canadian C-spine Rules. Each of these
systems allows you to either move toward clinical clearance of the C-spine or escalate
evaluation to spine imaging.
Canadian C-Spine rules
These rules help one decide if spine imaging is indicated. First, consider any high-risk
features; if none, examine any low risk features. If after considering all of the features, and
none apply, the patient can be cleared clinically, and the cervical spine immobilization can be
discontinued.
Canadian High-risk Features
10
Are there any high-risk factor that mandates radiography?
• Age > 65 yrs. or dangerous mechanism (fall from elevation over 3 feet or 5 stairs)?
• An axial load to the head (e.g. diving)?
• A motor vehicle collision exceeding 100 km/hr (63 miles/hr) or with roll-over or
ejection, or a collision involving a motorized recreational vehicle, or a bicycle
collision?
IF YES to ANY of the above, consider CT criteria for imaging next.
If NO to ALL of the above, move on to Canadian Low Risk features below.
Canadian Low-risk Features

Do any of the following low risk features exist?
• Simple rear-end motor vehicle collision
• Sitting position in the emergency department
• Ambulatory at any time
• Delayed (not immediate) onset of neck pain
• Absence of midline cervical-spine tenderness
If YES to ANY of the above, then proceed to testing of neck rotation.
If NO to ALL of the above, then consider CT criteria for clearance.
NEXUS rules:
5 questions
NEXUS Rules: These "rules" apply 5 criteria that used alone can help you clinically clear the
cervical spine. These include the presence of spinal tenderness and presence of focal
neurological deficit among other things. Use of the NEXUS rules is a reasonable protocol to
clear the cervical spine; although we encourage you to look at the Canadian Rules as well.
The NEXUS rules are:

• No posterior midline cervical-spine tenderness.
• No evidence of intoxication.
• A normal level of alertness.
• No focal neurological deficit.
• No painful distracting injuries.
If all of the above are true, then you can clinically clear the cervical spine and remove the
immobilization device. If any one or more is true, move on to the next step regarding spine
imaging.
11
Image the C-Spine With CT

CT is most sensitive for bony injury
The patient meets criteria for CT imaging of the spine. Maintain C-spine immobilization
throughout the imaging and transportation.
CT imaging positive: reveals a fracture or suspicious Injury
The CT reveals a finding that is definitive (vertebral fracture) or suspicious (soft tissue
swelling).
• Maintain C-spine immobilization
• Consult Spine surgeon (Neurosurgery or Orthopedic Surgery)
CT shows no fracture: no fracture or soft tissue swelling
The CT shows intact vertebrae and no evidence for soft tissue swelling around the spine. At
this point it is okay to move toward clinical clearance of the cervical spine if possible.
12
Consider MRI imaging
Obtain MRI as indicated
• If neurological examination is compatible with spinal cord injury (myelopathy) or the

patient complains of bilateral paresthesias (including painful dysthesthesias)
• If the patient is alert with continued midline cervical spine tenderness or if the patient
is expected to require prolonged cervical spinal immobilization (e.g. severe closed
head injury), consider MRI for the possibility of anterior-posterior spinal ligamentous
injury
• Perform MRI of the known or suspected areas of spinal cord injury
13
Initial Treatment of TSI

No steroids
The mainstay of treatment for TSIs is:

• Once a fracture has been diagnosed, the patient should be maintained with spinal
motion restriction during all treatments. As opposed to patients with spinal column
injuries without deficit or patients with TL injuries, patients with cervical TSIs often
have life threatening issues that are a direct consequence of their spine injury.
• Closed or open reduction of any identified spinal misalignment that leads to spinal
cord compromise
• Decompression of the spinal cord to minimize additional injury from cord
compression (this may include removal of hemorrhages or ruptured discs)
• Surgical stabilization of unstable ligamentous and bony injury
• Minimize the effect of secondary complications, such as venous thromboembolic
disease, pressure ulcer prevention, respiratory failure, and infections.
• Steroids: The use of steroids following acute traumatic cervical spinal injury should
not be considered the standard of care. Fifteen medical societies, including the
American Association of Neurological Surgeons and the Congress of Neurological
Surgeons do not recommend their use. Methylprednisolone therapy is not Food and
Drug Administration (FDA) approved for this application. Steroid use is associated
with increased complications such as pneumonia and gastrointestinal bleeding, as
well as hyperglycemia in diabetic patients.
• Adequate fluid resuscitation and treatment of neurogenic shock is essential.
14
Maintain Spinal Precautions

Focus on stabilization until injury is confirmed absent
Appropriate care must be taken to provide spinal immobilization on scene. The spinal column
should be immobilized until an unstable injury can be excluded. In the prehospital setting,
patients are typically fitted with a cervical collar to provide cervical spinal column
immobilization, and patients are subsequently transferred to the hospital on a backboard. If the
patient is intoxicated and uncooperative with medical evaluation, chemical sedation may be
indicated to assure proper protection of the spinal column and, more importantly, the spinal
cord. The patient should be removed as soon as possible from the backboard, ideally at the
conclusion of the primary or secondary survey. Evidence suggests leaving a patient on a
backboard can lead to deleterious complications such as skin breakdown.
As a general rule, the diagnosis and treatment of the majority of spine injuries can be deferred
to address other life-threatening injuries, such as hemorrhage or intracranial mass lesions, as
long as spine immobilization is maintained.
Brief Neurological Examination
As part of initial trauma survey, evaluate for motor/sensory deficit
In the primary survey of trauma patients, the neurologic assessment can be abbreviated to
include the patient's Glasgow Coma Scale (GCS), pupil size and reactivity, ability to move all
four extremities, and any spinal cord injury level.
15
Neurological Examination
Focus on signs related to spinal cord injury
The neurological examination should focus on motor, sensory and rectal tone findings. If the
patient has abnormality in any of these, the goal is to localize the lesion to the highest spinal
level where you see dysfunction.
Neurological signs present? Clinical findings supporting spine injury:
Based on a neurological examination, there are findings consistent with a spinal cord injury.
They include:
• Weakness below the level of the spine injury
• Sensory loss below the level of spine injury
• Loss of rectal tone
• Hyperreflexia or areflexia
• Priapism
If present, one should image the spine with CT and maintain spine immobilization.
Detailed examination
Here are a few motor and sensory "levels" as a guide (these refer to the myotome and
dermatome respectively for these regions of dysfunction):
Ten key muscles that should be tested and documented (grade each as grade 0-5*):
• C5- Biceps
• C6 - Extensor carpi radialis longus
• C7 - Triceps
• C8 - Flexor digitorum profundus
• T1 - Adductor digiti minimi
• L2 - Iliopsoas
• L3 - Quadriceps
• L4 - Tibialis anterior
• L5 - Extensor hallucis longus
• S1 - Gastrocnemius, soleus
• Sacral: voluntary anal contraction (present/absent)
*Motor Strength Grading:

• 0 = no active movement
• 1 = muscle contraction
• 2 = movement thru ROM w/o gravity
16
• 3 = movement thru ROM against gravity
• 4 = movement against some resistance
• 5 = movement against full resistance
Detailed examinations recommended by the American Spinal Injury Association can be found
on their website.
Sensory:
• C4 - deltoid
• T4 - nipple
• T10 - umbilicus
Decreased rectal tone:

• May be the only sign of a spinal cord injury
Sensory examination: Is there a sensory level?
With light touch and/or pin, touch each dermatome beginning with C1 (posterior scalp) and
move caudally to see if the patient has normal, diminished or absent sensory function at a
particular level and below. Light touch and pain may be separated by 1-2 dermatomes; select
the highest (cephalad) level as the sensory level. Test sacral sensory function with a pin;
score it as normal, diminished or absent. Score deep anal sensation as present or absent.
Specific syndromes: depending on the level and nature of injury
There are several spinal cord injury syndromes that, if present, help indicate the extent and
nature of the injury.
• Anterior Cord Syndrome - Loss of pain/temperature and motor but not light touch;
due to contusion of the anterior cord or occlusion of the anterior spinal artery. It is
associated with burst fractures of the spinal column with fragment retropulsion by the
axial compression.
• Central Cord Syndrome - Loss of cervical motor function with relative sparing of
lower extremity strength. This is typically due to hyperextension injury in elderly
patients with cervical stenosis. It is often not associated with a fracture; rather,
buckling of the ligamentum flavum contuses the cord causing bleeding and/or
ischemia within the center of the cord. The amount of damage to the corticospinal
tracts (which lie laterally) is variable and determines the amount of lower extremity
weakness.
• Brown-Sequard Syndrome - Hemiplegia, loss of ipsilateral light touch, and loss of
contralateral pain/temperature sensation due to hemisection of the cord. Indicates a
penetrating cord injury often from missile or knife, or a lateral mass fracture of the
spine or a protruding disc causing lateral compression.
17
ASIA Impairment scale: important for prognosis
The American Spinal Injury Association (ASIA) defined a 5-element scale that is prognostic of
neurological recovery:
A - Complete: No motor or sensory function in the lowest sacral segment.
B - Incomplete: Sensory but not motor function is preserved in the lowest sacral
segment.
C - Incomplete: Less than one-half of the key muscles below the neurological spinal
level have grade 3 or better strength.
D - Incomplete: at least one-half of the key muscles below the neurological level have
grade 3 or better strength.
E - Sensory and motor function are normal.
Complete injury (no sensory or motor function below a spinal level) has a worse prognosis;
however, spinal shock can confound the initial clinical exam. Incomplete injuries have better
prognosis for functional recovery.
18
Acute Non-traumatic Weakness Protocol
Version 4.0
Authors
Aimee M. Aysenne, MD, MPH
Shahana Uddin, MBBS, MD

Acute Non-traumatic Weakness Algorithm
(click each box to view details)

Checklist
☐ Assess and manage airway, breathing, and circulation
☐ Characterize the weakness by neurological exam
☐ Localize the lesion to create a differential diagnosis of the causes of weakness
☐ Initial labs: Glucose, electrolytes, Ca, Mg, PO4, BUN/Cr, LFTs, PT, PTT, CBC, and ABG
☐ Special Labs: TFTs, CPK or CK, ESR, parathyroid hormone, GGT
☐ Relevant MRI and CT imaging
Communication
☐ Salient history and exam findings
☐ Airway status and any respiratory issues
☐ Relevant labs and imaging (if done)
☐ Cause of weakness if known; differential diagnosis if not known
☐ Treatments provided
☐ Trajectory of disease process including last known well time.
3
Acute Weakness
Patients presenting with any form of new weakness
This topic provides an organized approach to the patient with new weakness not associated
with or caused by trauma. If the patient has experienced trauma follow the links to the ENLS
protocols Traumatic Brain Injury and Traumatic Spine Injury as appropriate.
Based on the patient’s pattern of weakness, one can decide the degree of urgency for airway
and ventilatory support as well as the need for administration of time-sensitive treatments such
as intravenous thrombolytic. Determining the pattern of weakness and associated findings on
clinical history and exam help to localize the anatomical lesion. Each anatomical lesion has
different disease processes that affect that location
4
Establish LKW Time (Date and Time)

If possible, asking the patient or a witness the timeline of onset, where the person is weak, if
there are any sensory symptoms including numbness or tingling, and any associated
symptoms is helpful. For children, a developmental and family history obtained from the
parents may help in early evaluation for the first acute presentation of metabolic or
neurodegenerative disorder with muscle weakness.
5
Establish Affected Anatomical Region

Perform a neurological examination on the patient that includes:
• Mental Status – alterations in consciousness? Speaking ability?
• Cranial Nerves – note whether abnormal pupils and eye movements, facial weakness,
poor gag and cough reflexes (oropharyngeal weakness), or neck weakness
• Motor
o Strength testing of proximal and distal extremity muscles, and compare flexor
versus extensor muscle strength, noting symmetry between sides
o Judge diaphragmatic and chest wall muscle strength to determine if there is any
respiratory insufficiency (single breath count from 1 to 20 [external intercostal
muscles] and maximal inspiratory pressure or negative inspiratory force
[diaphragm].)
• Sensory exam – determine the presence or absence of sensory signs
• Deep tendon reflexes
Table: These are usual findings for five anatomical localizations of weakness
Sensory Pattern of weakness

symptoms/signs
Localization Reflexes
Brain/spinal cord sometimes increased distal > proximal
extensors > flexors
Anterior Horn Cell never increased in ALS; Proximal and distal;
decreased in polio prominent atrophy
and fasciculations
Spinal nearly always decreased follows nerve
nerve/peripheral innervation
nerve
Neuromuscular never normal, decreased if proximal; first eye
junction muscle is paralyzed muscles, neck
extensors, pharynx,
diaphragm, followed
by more generalized
weakness
Muscle never normal, unless muscle proximal
severely weak
6
Assess Airway, Breathing, Circulation; Check Blood Sugar
Assess the patient's airway and potential need for assisted ventilation
Periodically assess airway and muscles of respiration, as the condition may change over time.
If any of the following general, subjective or objective findings are present, consider intubation.
General:
• Increasing generalized muscle weakness
• Dysphagia
• Dysphonia
• Dyspnea on exertion and at rest
Subjective:
• Rapid shallow breathing
• Tachycardia
• Weak cough
• Interrupted or staccato speech (gasping for air)
• Use of accessory muscles
• Abdominal paradoxical breathing
• Orthopnea (difficult or painful breathing except when erect)
• Weakness of trapezius and neck muscles: inability to lift head
• Inability to perform a single-breath count: count from 1 to 20 in single exhalation
(Forced vital capacity 1.0 L is roughly equal to counting from 1 to 10)
• Cough after swallowing
Objective:
• Decreased level of consciousness (have a lower threshold to control the airway if
the patient requires transfer or movement to unmonitored areas)
• Hypoxemia
• Vital capacity (VC) < 1 L or 20 ml/kg, or 50% decrease in VC in a day
• Maximum inspiratory pressure > -30 cm H2O
• Maximum expiratory pressure < 40 cm H2O
• Nocturnal desaturation
• Hypercarbia (a late finding)
Special Considerations for Intubation
• Rapid sequence induction/intubation is advised.

• Avoid use of succinylcholine if there is evidence of underlying progressive
neuromuscular disease (precipitates acute hyperkalemia) such as Guillain-Barré,
chronic neuromuscular weakness, or prolonged immobilization. Consider 1.0 – 1.4
mg/kg rocuronium as an alternative.
7
• Succinylcholine will be relatively ineffective to achieve muscle relaxation in
myasthenia gravis, unless a higher dose is used (~2.5 times the standard dose).
Conversely it is recommended to use half-dose of a non-depolarizing agent
(rocuronium 0.5-0.6 mg/kg) in such patients because they may be more sensitive to
nondepolarizing neuromuscular junction blockers.
• Consider non-invasive assisted ventilation as a temporizing measure in a
neurologically stable patient, while the diagnosis is established or with a known
neuromuscular condition expected to have a rapid resolution (e.g., myasthenia
gravis exacerbation).
• Prepare atropine/glycopyrrolate, fluids, and vasopressors if there is evidence of
autonomic instability.
See ENLS protocols Airway, Ventilation and Sedation and Pharmacotherapy.
Blood sugar
Always assess a blood sugar level and treat hypoglycemia.
8
Use Neurological Exam to Localize Lesion

Assess if the patient has global weakness or an upper or lower motor neuron injury.
Exam component Key Maneuvers and Findings

State of Interaction with examiner
consciousness Glasgow Coma Scale
FOUR score
Language Following verbal commands, naming, repeating, and
reading
Cranial nerves Follow the examiner’s finger in an H pattern
Ask the patient to smile
Protrude the tongue
Say “ah” while observing the movements of the palate
and uvula
In an intubated patient, in-line suction catheter and oral
suction catheter can test cough and gag reflexes
Motor strength Lift the arms and legs
Pronation of the arms when held in an extended position
Detailed motor strength testing of each muscle group
Single breath count for muscles of respiration
Tone Passively move the neck, arms and legs: may be either
increased or decreased (flaccid)
Reflexes Rapidly tap on the tendon of a muscle
Sensory Different modalities include pain/temperature, light

touch, vibration, and proprioception
Pain and light touch in emergencies
Coordination Finger to nose to finger
Heel to shin
Perform a neurological examination on the patient that includes:

• Mental Status
o Alterations in consciousness? State of consciousness is easily assessed on
every patient based on his or her ability to interact with the examiner. The
Glasgow Coma Scale (GCS) and the FOUR score formalize these findings and
add a quantitative measurement.
o Speaking ability? Formal language testing may be limited in an emergency
situation but may include the ability to follow verbal commands, naming,
repeating, and reading when the situation is more stabilized.
• Cranial Nerves: The cranial nerves control the movements of the face.
9
o Abnormal pupils and eye movements? Having the patient follow the examiner’s
finger in an H pattern tests extraocular eye movements.
o Facial weakness? Ask the patient to smile, protrude the tongue, and say “ah”
while observing the movements of the palate and uvula test the remaining cranial
nerves.
o Poor gag and cough reflexes (oropharyngeal weakness)? In an intubated patient,
an in-line suction catheter and oral suction catheter can test cough and gag
reflexes.
o Neck weakness?
• Motor: Interpretation of the motor exam should account for the patient’s age, capacity to
understand commands, and degree of cooperation. In infants, the exam will rely
primarily on observation.
o Strength testing of proximal and distal extremity muscles, and compare flexor
versus extensor muscle strength, noting symmetry between sides
o Judge diaphragmatic and chest wall muscle strength to determine if there is any
respiratory insufficiency (single breath count from 1 to 20 [external intercostal
muscles] and maximal inspiratory pressure or negative inspiratory force
[diaphragm].)
• Sensory exam – determine the presence or absence of sensory signs, eg
pain/temperature, light touch, vibration, and proprioception. In an emergency situation,
light touch and pain are most useful and can be done quickly by running a soft material
along the patient’s skin or, if a greater degree of stimulation is required for testing,
pinching the patient can be used. Care must be taken to not injure the skin by twisting
or puncturing
• Deep tendon reflexes - tested by rapidly tapping on the tendon of a muscle to watch for
response.
10
Global Weakness
Acute generalized weakness may occur due to acute metabolic disorders including sepsis,
electrolyte disturbances, anemia, or endocrine disorders.
• Marked hyperglycemia may rarely present with an acute hemiplegia, but the majority of
electrolyte disorders result in symmetric involvement.
• Hypoglycemia must be excluded early, but it should be noted that most of these patients
are confused or have a decreased level of consciousness.
• Other electrolyte causes that must be considered include hyponatremia and

hypernatremia (Table 17), hypermagnesemia (Table 18), and hypophosphatemia (Table
19).
• Thyroid function studies may be helpful.
• Specific vitamin deficiencies can cause generalized weakness but are usually not
emergent.
• Central nervous system infection (meningitis, encephalitis, encephalomyelitis) may
cause weakness and is diagnosed with lumbar puncture. See ENLS Meningitis and
Encephalitis module.
• A postictal patient or a patient in status epilepticus can also present with focal or
generalized weakness. See ENLS Status Epilepticus module. There is typically little
confusion about the diagnosis, but if there is no history available leading up to the
presentation of a weak patient, the diagnosis may be more elusive.
• Acute weakness is also a prominent feature of certain organophosphate toxicity and

envenomations, though the latter is exceedingly rare (see Tables 26 and 27).
• Specific drugs may cause acute weakness including slow clearance of neuromuscular
blocker given during intubation.
11
Obtain Initial Labs

Initial: Glucose, electrolytes, Ca, Mg, PO4, BUN/Cr, LFTs, PT, PTT, CBC, and ABG
Special: TFTs, CPK or CK, ESR, parathyroid hormone, GGT
12
Obtain CT or Relevant Imaging

MRI or CT imaging with and without contrast as renal function allows may need to be
emergently obtained. Depending on the likely differential diagnosis and local healthcare
systems, transfer to an appropriate facility with the necessary imaging modalities and/or
relative medical expertise will need to be considered at various points in this initial
assessment.
13
Upper Motor Neuron (UMN) Signs

In well-established UMN lesions (brain and spinal cord), hyperreflexia, increased extremity
tone, and a positive Babinski sign (great toe extension with lateral plantar stimulation) are seen
on examination.
Note: The anterior horn of the spinal cord houses the connection between the upper and lower
motor neurons. Conditions that affect these cells can cause exam findings of both UMN and
LMN and spare sensory neurons. There is a limited number of disease processes that affect
this area: amyotrophic lateral sclerosis (ALS) or “Lou-Gehrig’s disease”, enterovirus D68, polio,
and West Nile virus. These are rare conditions and require expert consultation where
available. Only 29 cases of polio have been reported worldwide in 2018.
14
Brain – if consciousness or facial movement

Brain lesions or global metabolic processes such as toxins may affect consciousness.
If the patient has signs and symptoms consistent with acute stroke such as abrupt onset of
hemiparesis and is within the time window for intravenous thrombolysis or endovascular
therapy, see the emergency evaluation of ENLS: Acute Ischemic Stroke.
15
Consider Stroke Pathway

Within the time window?
If the patient has signs and symptoms consistent with acute stroke such as abrupt onset of
hemiparesis and is within the time window for intravenous thrombolysis or endovascular
therapy, see the emergency evaluation of ENLS: Acute Ischemic Stroke.
16
Obtain Initial Labs and Imaging

Initial labs: Glucose, electrolytes, Ca, Mg, PO4, BUN/Cr, LFTs, PT, PTT, CBC, and ABG
Special labs: TFTs, CPK or CK, ESR, parathyroid hormone, GGT
Imaging: MRI or CT imaging with and without contrast as renal function allows may need to be
assessment.
17
Spinal Cord
Quadraparesis/Paraparesis
• Transverse myelitis (Table 15)
• Spinal cord compression
• Acute West Nile virus associated paralysis
• Spinal cord infarction (Table 16)
• Syrinx
• Drug ingestion (nitrous oxide inhalation)
• Generalized weakness: electrolyte and glucose abnormalities (Tables 9, 10, 17, 18, 19)
Quadriparesis/plegia is symmetrical weakness of all four limbs. Paraparesis/plegia is a

symmetrical weakness of both lower limbs. Often, this is related to a spinal cord dysfunction.
See ENLS: Spinal Cord Compression module.
18
See Spinal Cord Pathway

Quadraparesis/Paraparesis
• Transverse myelitis (Table 15)
• Spinal cord compression
• Acute West Nile virus associated paralysis
• Spinal cord infarction (Table 16)
• Syrinx
• Drug ingestion (nitrous oxide inhalation)
• Generalized weakness: electrolyte and glucose abnormalities (Tables 9, 10, 17, 18, 19)
Quadriparesis/plegia is symmetrical weakness of all four limbs. Paraparesis/plegia is a

symmetrical weakness of both lower limbs. Often, this is related to a spinal cord dysfunction.
See ENLS: Spinal Cord Compression module.
19
Lower Motor Neuron (LMN) Signs

LMN lesions (from the anterior horn cells in the spinal cord to the muscles) cause a flaccid,
areflexic weakness and, with time, atrophy and fasciculations (involuntary contractions or
twitching of muscle fibers).
Note: The anterior horn of the spinal cord houses the connection between the upper and lower
motor neurons. Conditions that affect these cells can cause exam findings of both UMN and
LMN and spare sensory neurons. There is a limited number of disease processes that affect
this area: amyotrophic lateral sclerosis (ALS) or “Lou-Gehrig’s disease”, enterovirus D68, polio,
and West Nile virus. These are rare conditions and require expert consultation where
available. Only 29 cases of polio have been reported worldwide in 2018.
20
Confirm time course – if acute, consider UMN and LMN
In the acute phase, UMN lesions may mimic a LMN lesion: flaccid paralysis, normal or reduced
tone, and unreliable reflexes. There is often not enough time for atrophy to be evident, and
fasciculations are rarely seen.
21
Nerve
Peripheral nerve syndromes can cause acute weakness. Compression including compartment
syndrome is a common cause. Knowledge of the innervation of each nerve is paramount to
making the diagnosis. When more than one peripheral nerve has been affected, this is called
mononeuropathy multiplex and is more commonly a vasculitic immune mediated process.
These conditions are rarely neurological emergencies.
Localization Pattern of Sensory Reflexes Acute

Weakness Loss Etiologies
Peripheral In the Variable Absent or Guillain-Barre
nerve distribution of Decreased syndrome
the nerve, or Vasculitic
diffusely neuropathy
present as Toxin-induced
stocking/glove nerve
weakness compression
syndromes
Acute diabetic
lumbosacral
radiculoplexus
neuropathy
22
Neuromuscular Junction
Neuromuscular First in eye Absent Normal, Myasthenia
junction muscles, neck decreased if gravis, Lambert-
extensors or muscle is Eaton
flexors, paralyzed myesthenic
pharynx, syndrome,
diaphragm, Botulism, tick
followed by bite,
more organophosphat
generalized e toxicity
weakness
23
Muscle
Muscle Proximal Absent Normal Acute
unless myopathy,
muscle Rhabdomyolysi
severely s, Myositis
weak
24
Consider Differential Diagnosis

A detailed history and comprehensive neurological exam are important but may not be
practical in the prehospital and immediate resuscitation period, and may be completed when
the patient’s airway and ventilation have been stabilized. However, at a minimum, obtain the
patient’s last known well time and perform a brief neurological exam to form a workable and
realistic list of differential diagnoses. If possible, asking the patient or a witness the timeline of
onset, where the person is weak, if there are any sensory symptoms including numbness or
tingling, and any associated symptoms is helpful. For children, a developmental and family
history obtained from the parents may help in early evaluation for the first acute presentation of
metabolic or neurodegenerative disorder with muscle weakness.
25
Confirm Airway and Ventilation with Expected Time Course of

Disease Process
Assess the patient's airway and potential need for assisted ventilation
Periodically assess airway and muscles of respiration, as the condition may change over time.
If any of the following general, subjective or objective findings are present, consider intubation.
General:
• Increasing generalized muscle weakness
• Dysphagia
• Dysphonia
• Dyspnea on exertion and at rest
Subjective:
• Rapid shallow breathing
• Tachycardia
• Weak cough
• Interrupted or staccato speech (gasping for air)
• Use of accessory muscles
• Abdominal paradoxical breathing
• Orthopnea (difficult or painful breathing except when erect)
• Weakness of trapezius and neck muscles: inability to lift head
• Inability to perform a single-breath count: count from 1 to 20 in single exhalation
(Forced vital capacity 1.0 L is roughly equal to counting from 1 to 10)
• Cough after swallowing
Objective:
• Decreased level of consciousness (have a lower threshold to control the airway if
the patient requires transfer or movement to unmonitored areas)
• Hypoxemia
• Vital capacity (VC) < 1 L or 20 ml/kg, or 50% decrease in VC in a day
• Maximum inspiratory pressure > -30 cm H2O
• Maximum expiratory pressure < 40 cm H2O
• Nocturnal desaturation
• Hypercarbia (a late finding)
Special Considerations for Intubation
• Rapid sequence induction/intubation is advised.
26
• Avoid use of succinylcholine if there is evidence of underlying progressive
neuromuscular disease (precipitates acute hyperkalemia) such as Guillain-Barré,
chronic neuromuscular weakness, or prolonged immobilization. Consider 1.0 – 1.4
mg/kg rocuronium as an alternative.
• Succinylcholine will be relatively ineffective to achieve muscle relaxation in
myasthenia gravis, unless a higher dose is used (~2.5 times the standard dose).
Conversely it is recommended to use half-dose of a non-depolarizing agent
(rocuronium 0.5-0.6 mg/kg) in such patients because they may be more sensitive to
nondepolarizing neuromuscular junction blockers.
• Consider non-invasive assisted ventilation as a temporizing measure in a
neurologically stable patient, while the diagnosis is established or with a known
neuromuscular condition expected to have a rapid resolution (e.g., myasthenia
gravis exacerbation).
• Prepare atropine/glycopyrrolate, fluids, and vasopressors if there is evidence of
autonomic instability.
See ENLS protocols Airway, Ventilation and Sedation and Pharmacotherapy.
27
Send Confirmatory Labs and Studies

Send all relevant information.
Initial labs: Glucose, electrolytes, Ca, Mg, PO4, BUN/Cr, LFTs, PT, PTT, CBC, and ABG
Special labs: TFTs, CPK or CK, ESR, parathyroid hormone, GGT
Imaging: MRI or CT imaging with and without contrast as renal function allows may need to be
assessment.
28

Emergency Neurological Life Support, Protocols.2019.4th Ed

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Emergency Neurological Life Support

Acute Ischemic Stroke Protocol

Last updated: October 2019

Protocol developed by: Noah Grose, BSN, MSN, ACNP-BC

Checklist & Communication

Acute Ischemic Stroke Algorithm ...............................................................................................1

Sample Sign-Off Narratives

Acute Ischemic Stroke

After placing two peripheral IV lines:

Hospital Admit or Transfer

If tPA was administered:

Watch for complications of tPA, including

o Steroids, e.g. methylprednisolone 125 mg IV

Consider patient transfer if:

Low Risk TIA

No tPA unless BP is reduced

Blood pressure (BP) exceeds 185/110 mmHg

If BP falls below 185/110 mmHg, proceed to IV tPA administration.

***Permissive hypertension is allowed for TIA, as it is for non-tPA treated patients, up to

High Risk TIA

Admit for observation:

Onset Less Than 3 hours

Time from stroke symptom onset is less than 3 hours

Time of onset is when the patient was last seen normal.

Check eligibility for on-label (US and elsewhere) use of IV tPA:

Absolute Exclusion Criteria if positive:

• No history of intracranial neoplasm, aneurysm, or arteriovenous malformation. Note

Relative Exclusion Criteria if positive:

Some additional considerations:

Onset Between 3 and 4.5 Hours

Time of onset is when the patient was last seen normal.

• Meet all criteria of < 3 hours since stroke onset

Patient improves following tPA

Yes - Patient is an IV tPA Candidate

No - Patient is not an IV tPA or IA Treatment Candidate

Symptom Onset > 4.5 hours

The ABCD2 Score

ABCD2 Element Points

Total risk ABCD2 Score 2 day 7 day 90 day

Ref: Cucchiara B et al, Ann Emerg Med 2008, 52:S27-39

Last updated: October 2019

Protocol developed by: Venkatakrishna Rajajee, MBBS

Checklist and Communication

Intubation - does the patient need to be intubated?

Document focused neurological assessment

Exam should include:

A difficult airway may be broadly defined as an endotracheal intubation attempt in which a

The "MOANS" mnemonic helps predicts ease of bag-mask ventilation:

The "LEMON" mnemonic helps to predict difficult tracheal intubations:

PATIENT EQUIPMENT TEAM

1. RELIABLE IV/ IO ACCESS 1. MONITORING 1. ASSIGN ROLES

Algorithm for endotracheal intubation

Intubation Sequence for Elevated ICP

Goals of mechanical ventilation

Immediately following intubation, respiratory and hemodynamic homeostasis should be

Ideal Body Weight:

Occasionally, severe intracranial hypertension, status epilepticus, or the need for

Dexmedetomidine: Dexmedetomidine is a centrally acting alpha-2 agonist Desirable

Last updated: October 2019

Protocol developed by:

Checklist & Communication

Sample Sign-off Narrative: