University of Regina Carmeli

City of Malolos, Bulacan

College of Allied Medical Sciences

A Case Study of Hypoxic Encephalopathy

Submitted by:

Martin, Mutya S.

Musni, Chino G.

BSN 4B Group 3

September 21, 2010

NURSING HISTORY

History of present illness/ active problem

Patient was diagnosed of Hypoxic encephalopathy due to hypocolemic shock 2’

to massive blood loss, S/P “E” wound exploration and ligation of bleeders (Dec. 29,
2008).

According to the patient it was December 2008 when they were in duty at Negros
Occidental, Mr. GP and his friend met a man who have a knife with him and when this
man stabbed his friend he tried to cover and parried it with his arm that cause him
severe bleeding. He lost too much blood that cause eight (8) days comatose to him.

Family Medical History

(+) HTN in father side.

Previously smoker and drinker.

PERSONAL INFORMATION

Name: Mr. G P

Rank: Sgt

Birth Date: June 26, 1965

Age: 43 years old

Address: Calumpang Salong Kabankalan City Negros Occidental

Religion: Roman Catholic

Date Admitted: April 21, 2010

NEUROLOGICAL ASSESSMENT

Glasgow Coma Scale

EYES VERBAL MOTOR

1 Does not open eyes
2 Opens eyes in response to
painful stimuli
3 Opens eyes in response to
voice
4 Opens eyes spontaneously
5 N/A
6 N/A
Score 4 5
Makes no sounds Makes no movements
Incomprehensible sounds Extension to painful stimuli
(decerebrate response)
Utters inappropriate words Abnormal flexion to painful
stimuli (decorticate
response)
Confused, disoriented Flexion / Withdrawal to
painful stimuli
Oriented, converses Localizes painful stimuli
normally
N/A Obeys commands
6

Total Score: 15

Note: Right and Left Upper Extremities and Left Lower Extremities

Muscle Strength and Tonicity

2 0
2

5 0

A stick figure may be used to record muscle strength as follows:

5
5: Full range of motion against gravity and resistance 0
 4: Full range of motion against gravity and a moderate amount of resistance

3: Full range of motion against gravity only

2: Full range of motion when gravity is eliminated

1: A weak muscle contraction when muscle is palpated, but no movement

0: complete paralysis

Cranial Nerve Test

NERVE NAME FUNCTION TEST RESULT

I Olfactory Smell Have athlete -Toothpaste

smell a familiar
-both nostrils are
odor
functioning well.

- Able to
recognize.

II Optic Visual Acuity Have athlete

identify fingers
Visual Field Ok
Check peripheral
vision

III Oculomotor Pupillary Reaction Shine Light in - responds to

the eye
light, both pupils
constrict

- Eyes – the pt
follows
examiners
fingers as it
move in all
direction.
IV Trochlear Eye Movement Follow finger -able to touch
without moving
the head -both side of the
mouth
manifested
muscle strength
when tested by
tongue
depressor

V Trigeminal Facial Sensation Touch the face (same as

Trochlear CN IV)
Motor Function Have athlete
hold mouth open

VI Abducens Motor Function Lateral Eye (same as

movements
Oculomotor CN
III)

VII Facial Motor Function Smile, wrinkle -with facial

face, puff cheeks
symmetry
Sensory
Tastes
- able to
recognize the
taste of the food

VIII Acoustic Hearing Snap fingers by stroke

the ear
Balance
Rhomberg's Test

IX Glossopharyngeal Swallowing and Voice Swallow and say With gag reflex
"AH"

X Vagus Gag Reflex Use tongue - able to say

depressor
“ah”, no deviation

XI Spinal Accessory Neck Motion Shoulder -able to fight the

shrugging
resistance
 applied by the
examiner

XII Hypoglossal Tongue Movement and Stick out tongue -able to move the
Strength apply resistance
tongue in
with a tongue
depressor different
directions.

GENERAL DESCRIPTION OF THE DISEASE

Hypoxic Encephalopathy is encephalopathy caused by hypoxia from decreased rate of

blood flow or decreased oxygen in the blood; severe cases can cause permanent brain damage
within five minutes.

ANATOMY AND PHYSIOLOGY

Brain

The human brain is the center of the

human nervous system and is a highly complex
organ. Enclosed in the cranium, it has the same
general structure as the brains of other
mammals, but is over three times as large as
the brain of a typical mammal with an equivalent
body size. Most of the expansion comes from
the cerebral cortex, a convoluted layer of neural tissue that covers the surface of the forebrain.
Especially expanded are the frontal lobes, which are associated with executive functions such
as self-control, planning, reasoning, and abstract thought. The portion of the brain devoted to
vision is also greatly enlarged in human beings.

The brain monitors and regulates the body's actions and reactions. It continuously
receives sensory information, and rapidly analyzes this data and then responds, controlling
bodily actions and functions. The brainstem controls breathing, heart rate, and other autonomic
processes that are independent of conscious brain functions. The neocortex is the center of
higher-order thinking, learning, and memory. The cerebellum is responsible for the body's
balance, posture, and the coordination of movement.

Spinal Cord

The spinal cord is a long, thin, tubular bundle of nervous tissue and support cells that
extends from the brain (the medulla specifically). The brain and spinal cord together make up
the central nervous system. The spinal cord extends down to the space between the first and
second lumbar vertebrae; it does not extend the entire length of the vertebral column. It is
around 45 cm (18 in) in men and around 43 cm (17 in) long in women. The enclosing bony
vertebral column protects the relatively shorter spinal cord. The spinal cord functions primarily in
the transmission of neural signals between the brain and the rest of the body but also contains
neural circuits that can independently control numerous reflexes and central pattern generators.
The spinal cord has three major functions: A. Serve as a conduit for motor information, which
travels down the spinal cord. B. Serve as a conduit for sensory information, which travels up the
spinal cord. C. Serve as a center for coordinating certain reflexes.

The spinal cord sends and receives

information from the entire body and brain .The
information controls sensations, movement, and
autonomic function. Nerves traveling through the
body relay the information from the spinal cord to
target cells in all areas of the body. Axon
bundles travel through the body in 2 pathways:
ascending and descending. The descending
pathway, which controls voluntary movement,
carries information from the corticospinal tract in
the brain to the motor neurons in the spinal cord and then to the final destination in the body.
Information carried by the ascending pathway from the sensory neurons in the spinal cord to the
brain controls sensory information about body position, temperature, pain, and touch . Each
level of the spinal cord corresponds to the sensory perception at a particular part of the body.
The lower the level of the spinal cord, the lower the area of the body that is controlled by that
level. Thus, the lower the level of the spinal cord injury, the lower the parts of the body that are
affected by the injury.
PATHOPHYSIOLOGY

Brain hypoxia and ischemia due to systemic hypoxemia, reduced cerebral blood flow

(CBF), or both are the primary physiological processes that lead to hypoxic-ischemic

encephalopathy. The initial compensatory adjustment to an asphyxial event is an increase in the

CBF due to hypoxia and hypercapnia. This is accompanied by a redistribution of cardiac output

such that the brain receives an increased proportion of the cardiac output. A borderline increase

in the systemic blood pressure (BP) further enhances the compensatory response. The BP

increase is due to increased release of epinephrine; these are classic early cardiovascular

compensatory responses to asphyxia.

In adults, CBF is maintained at a constant level despite a wide range in systemic BP.

This phenomenon is known as the cerebral autoregulation, which helps to maintain the cerebral

perfusion. The physiological aspects of CBF auto regulation has been well studied in perinatal

and adult experimental animals. In human adults, the BP range at which CBF is maintained has

been shown to be 60-100 mm Hg. However, such a range of BP in the human fetus and the
newborn infant has not been studied with much rigor due to limitations of human

experimentation in the fetus and newborn.

MEDICAL MANAGEMENT

a. Diagnostic Procedures

• CT scan -a scan that uses x-rays and computer software to make pictures of
your brain.
• MRI scan -a test that uses magnetic waves to make pictures of structures
inside the brain
• Electrocardiogram (EKG, ECG) -a test that records the heart’s activity by
measuring electrical currents through the heart muscle.
• Echocardiogram —a test that uses high-frequency sound waves (ultrasound)
to examine the size, shape, and motion of the heart.
• Blood tests, including arterial blood gases and blood glucose levels
• Electroencephalogram (EEG) -a test that records the brain’s activity by
measuring electrical currents through the brain.
• Ultrasound-a test that uses sound waves to evaluate blood flow in the vessels
going to the brain or within the brain.

b. Laboratory Procedures

• Serum electrolyte levels

a. In severe cases, daily assessments of serum electrolytes are valuable until

the infant's status improves. Markedly low serum sodium, potassium, and
chloride levels in the presence of reduced urine flow and excessive weight
gain may indicate acute tubular damage or syndrome of inappropriate
antidiuretic hormone (SIADH) secretion, particularly during the initial 2-3 days
of life.
b. Similar changes may be seen during recovery; increased urine flow may
indicate ongoing tubular damage and excessive sodium loss relative to water
loss
 • Renal function studies: Serum creatinine levels, creatinine clearance, and
BUN levels suffice in most cases.
• Cardiac and liver enzymes: These values are an adjunct to assess the
degree of hypoxic-ischemic injury to these other organs. These findings may
also provide some insight into injuries to other organs, such as the bowel.
• Coagulation system evaluation: This includes prothrombin time, partial
thromboplastin time, and fibrinogen levels.
• ABG: Blood gas monitoring is used to assess acid-base status and to avoid
hyperoxia and hypoxia as well as hypercapnia and hypocapnia.

c. Therapeutic Regiment

Phenobarbital (Luminal)

DOC when clinical or EEG seizures are noted; is continued on the basis of both EEG
findings and clinical status. In most cases, can be weaned and stopped during the first month of
life; however, treatment is continued for several months to 1 year in infants with persistent
neurological abnormalities and clinical or EEG evidence of seizures; EEG and clinical status
should guide decision. In high doses, has been used prophylactically by a few researchers, but
its efficacy has not been established. In infants who are heavily sedated or paralyzed,
phenobarbital may be used prophylactically at standard dose.

DOSING 20 mg/kg IV over 10-15 min as loading dose; in refractory cases,

additional 5-10 mg/kg IV as loading dose; followed by 3-5 mg/kg/d
PO/IV/IM/PR divided bid, to begin no earlier than 12-24 h after
loading dose;

INTERACTIONS May decrease effects of digitoxin, corticosteroids, carbamazepine,

theophylline, metronidazole, and anticoagulants (patients stabilized
on anticoagulants may require dosage adjustments if added to or
withdrawn from their regimen); coadministration with alcohol may
produce additive CNS effects and death; valproic acid may increase
phenobarbital toxicity; rifampin may decrease phenobarbital effects
CONTRAINDICATIONS Documented hypersensitivity; severe respiratory disease, marked
impairment of liver function, and nephritic patients

PRECAUTIONS May contain 10% alcohol and >60% propylene glycol May lead to
respiratory distress, thus respiratory status should be monitored;
immediate assisted ventilatory support should be available
Monitor serum therapeutic concentrations, which should be 15-30
mcg/mL; prolonged serum half-life during the first 1-2 wk of life may
cause drug accumulation, requiring adjustment of maintenance
doses, due to low GFR in the first week of life and ATN (if present)
Allowing serum concentrations of 40 mcg/mL is not a universally
accepted practice
Observe IV sites for extravasation and phlebitis

Phenytoin (Dilantin)

Usually the third DOC in neonatal seizures; may be used in patients with seizures that
do not respond to phenobarbital or lorazepam. Oral absorption is negligible for the first several
months of life.

DOSING 15-20 mg/kg IV over >30 min as loading dose; followed by 4-8 mg/kg
IV slow push q24h (may divide into 2-3 doses q8-12h); rate of
infusion not to exceed 0.5 mg/kg/min; flush IV line with 0.9% NaCl
before and after administration

INTERACTIONS Benzodiazepines, cimetidine, fluconazole, isoniazid, metronidazole,

miconazole, phenylbutazone, succinimides, sulfonamides,
omeprazole, trimethoprim, and valproic acid may increase phenytoin
toxicity
Phenytoin effects may decrease when taken concurrently with
barbiturates, diazoxide, rifampin, antacids, charcoal, carbamazepine,
theophylline, and sucralfate

CONTRAINDICATIONS Documented hypersensitivity; sinoatrial block, second- and third-

degree AV block, sinus bradycardia, or Adams-Stokes syndrome; IM
 administration

PRECAUTIONS May contain 40% propylene glycol and 10% alcohol; monitor serum
concentrations, which should be 6-15 mcg/mL; monitor for
bradycardia, arrhythmias, and hypotension during infusion; highly
unstable in IV solution, avoid using in central lines because of risk of
precipitation; incompatible in D5W or D10W or with dextrose plus
amino acids and lipids, most antibiotics, heparin, insulin, and many
other drugs (consult compatibility text); drug extravasation at IV site
may lead to severe local necrosis

Lorazepam (Ativan)

Second DOC for acute control of seizures refractory to phenobarbital.

By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may
depress all levels of CNS, including limbic and reticular formation.

DOSING 0.05-0.1 mg/kg/dose IV slow push over 2-5 min; doses repeated on
basis of clinical response (careful with repeat dosing because of
benzyl alcohol content)

INTERACTIONS CNS toxicity increases when used concurrently with alcohol,

phenothiazines, barbiturates, or MAOIs

CONTRAINDICATIONS Documented hypersensitivity; preexisting CNS depression and

hypotension

PRECAUTIONS
Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to

fetus

Precautions

IV contains PEG 400, propylene glycol, and benzyl alcohol; may

cause respiratory depression and rhythmic myoclonic jerking in
premature infants receiving lorazepam for sedation
Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is

dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that in
turn produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation
produced by higher doses.

DOSING 2-20 mcg/kg/min IV continuous infusion; begin at lower doses,

increase on basis of systemic BP appropriate for age and gestational
age

INTERACTIONS Phenytoin, alpha-adrenergic and beta-adrenergic blockers, general

anesthesia, and MAOIs increase and prolong effects of dopamine

CONTRAINDICATIONS Documented hypersensitivity; pheochromocytoma or ventricular

fibrillation

PRECAUTIONS
Pregnancy

C - Fetal risk revealed in studies in animals but not established or not

studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause tachycardia and arrhythmias; may increase pulmonary

artery pressure; may reversibly suppress prolactin and thyrotropin
secretion

d. Surgical Treatment

In cases of posterior cranial fossa hematoma, surgical drainage may be lifesaving if no

additional pathologies are present.
NURSING RESPONSIBILITIES

Supportive care in patients with hypoxic-ischemic encephalopathy

Most infants with severe hypoxic-ischemic encephalopathy need ventilatory support

during first days of life. Although animal data suggest that permissive hypercapnia may be
neuroprotective, no such evidence is available in newborn. Therefore, the role of mechanical
ventilation is to maintain the blood gases and acid-base status in the physiological ranges and
prevent hypoxia, hyperoxia, hypercapnia, and hypocapnia. Hypocapnia in particular may lead to
severe brain hypoperfusion and cellular alkalosis and has been associated with worse
neurodevelopmental outcomes.

Infants with hypoxic-ischemic encephalopathy are also at risk for pulmonary

hypertension and should be monitored. Nitric oxide (NO) may be used according to published
guidelines.

Perfusion and blood pressure management

Studies indicate that a mean blood pressure (BP) above 35-40 mm Hg is necessary to avoid
decreased cerebral perfusion. Hypotension is common in infants with severe hypoxic-ischemic
encephalopathy and is due to myocardial dysfunction, capillary leak syndrome, and
hypovolemia; hypotension should be promptly treated. Dopamine or dobutamine can be used to
achieve adequate cardiac output in these patients. Avoiding iatrogenic hypertensive episodes is
also important.

Fluid and electrolytes management

Because of the concern for acute tubular necrosis (ATN) and syndrome of inappropriate
antidiuretic hormone (SIADH) secretion, fluid restriction is typically recommended for these
infants until renal function and urine output can be evaluated. However, this recommendation is
not based on evidence from randomized controlled trials. Therefore, fluid and electrolyte
management must be individualized on the basis of clinical course, changes in weight, urine
output, and the results of serum electrolyte and renal function studies.

Treatment of seizures
 Hypoxic-ischemic encephalopathy is the most common cause of seizures in the neonatal
period. Seizures are generally self-limited to the first days of life but may significantly
compromise other body functions, such as maintenance of ventilation, oxygenation, and blood
pressure. Additionally, studies suggest that seizures, including asymptomatic electrographic
seizures, may contribute to brain injury and increase the risk of subsequent epilepsy

a. Priority in Nursing Diagnosis

Diagnosis of HIE is made based on the history and physical and neurological
examinations . Many of the tests are performed to assess the severity of brain injury and to
monitor the functional status of systemic organs. The results of the tests should be interpreted in
conjunction with the clinical history and the findings from physical examination. Cranial
ultrasound can also reveal internal hemorrhage; however, visualizations may be difficult in
routine ultrasound examination. A CT scan of the head can be useful to confirm cerebral edema
(obliteration of cerebral ventricles, blurring of sulci). Echocardiography (ECHO) also helps to
define myocardial contractility and the existence of structural heart defects,

b. Potential Problem

Any injury, complication, or condition that causes the brain to have a reduction in blood
flow and oxygen deprivation is a risk factor for HIE.

DRUG STUDY

There were no medications for our patient during our 3 – 11 shift at 7A.

DIET THERAPY

In most cases (particularly in moderately severe and severe hypoxic-ischemic

encephalopathy), the infant is restricted to nothing by mouth (NPO) during the first 3 days of life
or until the general level of alertness and consciousness improves. In addition, infants
undergoing hypothermia therapy should remain NPO until rewarmed. Enteral feeds should be
carefully initiated and the use of trophic feeds is initially advisable (about 5 mL every 3-4 h).
Infants should be monitored carefully for signs and symptoms of necrotizing enterocolitis, for
which infants with perinatal asphyxia are at high risk. Individualize increments in feeding volume
and composition.