COMPREHENSIVE

THEORY FOR RN

JISHA S ABRAHAM
RESPIRATORY SYSTEM

2
3
Acute Respiratory Failure

Occurs when insufficient oxygen is transported to the blood or

inadequate CO2 is removed from the lungs and the client’s
compensatory mechanisms fail.

Causes:
Mechanical abnormality of the lungs or chest wall
A defect in the respiratory control center in the brain
An impairment in the function of the respiratory muscles

O2 may reach the alveoli but cannot be absorbed or used properly,

resulting in a PO2 lower than 60mm Hg, arterial O2 saturation (SaO2)
lower than 90% or PaCO2 greater than 50mm Hg, contributes to
Hypoxemia.

Assessment:

Dyspnea
Headache
Restlessness
Confusion
Tachycardia
Hypertension
Dysrhythmias
Decreased level of consciousness
Alterations in respirations and breath sounds

Interventions:

4
Identify and treat the cause of the respiratory failure
Administer Oxygen to maintain the PaO2 level higher than 60-70 mm
Hg
High fowler’s position
Encourage deep breathing
Bronchodilators
Mechanical ventilation if necessary

Acute Respiratory Distress Syndrome

It occurs as a complication of some other condition; it is caused by a

diffuse lung injury and leads to extravascular lung fluid
The major site of injury is the alveolar capillary membrane
Intestitial edema causes compression
The ABG levels identify respiratory acidosis and hypoxemia
Chest X ray shows bilateral interstitial and alveolar infiltrates

Causes:
Sepsis
Fluid overload
Shock
Trauma
Neurological injuries
Burns
Disseminated intravascular coagulation
5
Drug ingestion
Aspiration
Inhalation of toxic substances

Assessment:

Tachypnea
Dyspnea
Decreased breath sounds
Deteriorating ABG levels
Hypoxemia despite high concentrations of delivered O2
Decreased Pulmonary compliance
Pulmonary infiltrates

Interventions:

Identify and treat the cause

Administer O2
High fowler’s position
Restrict fluid intake
Diuretics, anticoagulants or corticosteroids as prescribed
Prepare for Mechanical ventilation

Chronic Obstructive Pulmonary Disease

COPD is a disease state characterized by airflow obstruction caused by

emphysema or chronic bronchitis.
Progressive airflow limitation occurs, associated with an abnormal
inflammatory response of the lungs that is not completely reversible. It
leads to pulmonary insufficiency, pulmonary hypertension and cor
pulmonale
6
Assessment:
Cough
Exertional Dyspnea
Wheezing and crackles
Sputum production
Weight loss
Barrel chest
Use of accessory muscles for breathing
Prolonged expiration
Orthopnea
Cardiac Dysrhythmias
Congestion and hyper inflation seen on chest X ray
ABG levels indicates respiratory acidosis and hypoxemia
PFT demonstrates decreased vital capacity

Interventions:
Monitor vitals
Administer a low concentration O2 (1-2 L/min) through nasal prongs
Monitor Pulse oxymetry
Pursed lip breathing techniques
Record the color, amount and consistency of sputum
Suction if necessary
Monitor weight
Small frequent meals
High calorie, high protein diet with supplements
Fluid intake up to 3000ml/day unless contraindicated
High fowler’s position
Allow activity as tolerated

7
Bronchodialators, corticosteroids, mucolytics and antibiotics as
prescribed

Pneumonia

An inflammation of the pulmonary tissue including the interstitial

space, alveoli and broncheols
Edema associated with inflammation stiffens the lung. It decreases the
lung compliance and vital capacity and cause hypoxemia
Chest X-ray presents diffused patches throughout the lung or
consolidation in a lobe
Sputum c/s identifies organism
Increased WBC and ESR indicates infection
Assessment:
Chills
Increased temperature
Pluritic pain
Rhales and rhonchi
Wheezing
Use of accessory muscles (respiratory distress)
Cyanosis
Mental status changes
Frothy sputum
Implementation:
Administer oxygen
Monitor vitals
Encourage coughing and deep breathing with incentive spirometry
Position changes and ambulation to mobilize secretions

8
Semi fowlers position
Chest physio
Monitor the characteristics of sputum
Small frequent diet
Antibiotics
Antipyretics
Bronchodialators
Cough suppressants (codein)
Mucolytic agents
Expectorents

Tuberculosis

It is a highly communicable disease caused by myco bacterium

tuberculi.
It affects the upper lobes where O2 content is highest and other areas
such as brain, intestine, peritoneum, joints, liver and kidney.
TB has an insidious onset

MDR-TB: Multi Drug Resistant strain exists due to improper or non

compliant treatment programs which may cause the development of
mutations in the tubercle bacilli

Risk factors:

Alcoholism
IV drug use
Mal nutrition
Infection
Elderly, homeless, refugees
9
Low socio economic group
Child under 5 years of age
Living in crowded areas
Contact with infected individuals
HIV patients
Drinking unpasteurized milk
Transmission through airborne by droplet infection

Diagnosis:

Tuberculin Test
Chest X ray
Confirmatory Test: Sputum Culture (AFB)

Infected individuals received TB medication for 2-3 weeks has less

chance of infection.
Droplet enters the lungs and bacteria forms a tubercle lesion. Body’s
defence system encapsulates the tubercle, leaving a scar. If no
encapsulation, bacteria may enter the lymph system leading to
granulomatous inflammation. In active phase, TB causes necrosis and
cavitation in lesions leading to rupture and spread of necrosis and
damage. Primary lesions if reactivated become secondary infection
when re exposed to bacterium.

Clinical manifestation:
Asymptomatic initially
Fatigue and lethargy
Anorexia
Weight loss
Low grade fever
10
Chills
Night sweats
Persistent cough with mucoid and muco purulent sputum; occasionally
blood strain
Chest tightness and dull aching chest pain

Physical examination:
Chest X ray: Multi nodular infiltrate with calcification in the upper lobe
suggest TB
Sputum C/S
Mantoux test: Purified protein derivative 0.1 ml intradermally on
anterior arm. Induration 10mm or more in diameter after 48-72 hrs
after injection indicates positive for TB. HIV infected individuals will be
positive for TB if the induration is 5mm or more.
Once skin test is positive Chest X ray is done to confirm exposure to
the bacteria.

Management:
Hospitalized client: Respiratory isolation in well ventilated room. It
should have 6 exchange of fresh air per hour.
Client should wear mask when he goes outside the room. Nurse should
wear particular respirator.
If the client is not infectious, no need for isolation.
If 2 Sputum culture is negative, no need for isolation.
Food rich in Iron, protein and Vitamin C
Avoid exposure to dust.
Medication:
Active Tb is treated for 6 – 9 months; further longer for HIV patients

11
Individuals with exposure are treated with preventive INH for 9 -12
months

First line medication for TB (2-4 weeks):

Refampin: in empty stomach
secretions red in color
avoid alcohol – risk of hepato toxicity
Inj. Streptomycin
Ethambutol
Isoniazid(INH): Take along with Vitamin B6
Limit tyramine rich food such as cheese and diary
products
Avoid alcohol – wine and beer
Avoid banana and raisins
Avoid Caffeine and chocolate – cause Hypertension
It interferes with hormonal contraceptives
Use with caution in clients with Chronic liver disease,
alcoholism, renal impairment and clients on hepato toxic
medications

Second line Medication:

Capreomycin Sulfate
Ethionamide
Aminosalicylic acid
Cycloserine
Kanamycin – After food to reduce GI upset

12
Instruct the client not to skip food.

Chest Tube Drainage System

Returns negative pressure to the intra pleural Space.

Used to remove abnormal accumulation of air and fluid from the
pleural space.

Collection Chamber where the chest tube from the client connects to
the system. Drainage from the tube drains in to and collects in a series
of calibrated columns in this chamber.

Water seal chamber: The tip of the tube is under water allowing the
fluid and the air to drain the pleural space and preventing air from

13
entering in to the pleural space
Water oscillates (moves up as the client inhales and moves down as the
client exhales)
Continuous bubbling indicates an air leak in the chest tube system.

Suction control chamber provides the suction which can be controlled

to provide a negative pressure to the chest. This chamber is filled with
various levels of water to achieve the desired level of suction. Lung
tissue could be sucked in to the chest tube without this control.
Gentle bubbling in this chamber indicates that there is suction and it
doesn’t indicate that air is escaping from the pleural space.

Implementation:
Collection Chamber:
Monitor drainage. Notify the physician if the drainage is more than 100
ml/hr or the drainage becomes bright red (bleeding) or increases
suddenly.
Mark the chest tube drainage in the collection chamber at 1-4 Hrs
interval using a piece of tape.

Water seal chamber:

Monitor for the fluctuation of fluid level. Fluctuation in the chamber
stops if the tube is obstructed or if the suction is not working properly
or lungs have fully re expanded.
If the client has known pneumothorax intermittent bubbling in the
water seal chamber is expected as the air is drained from the chest but
continuous bubbling indicates an air leak in the system. Notify the
physician if there is continuous bubbling.

14
Suction control chamber:
Gentle bubbling is normal.
Vigorous bubbling is due to air leak

Implementation:
An occlusive sterile dressing is maintained at the insertion site.
Chest X ray to assess the position of the chest tube and determine
whether the chest is re expanded
Assess respiratory status and lung sounds
Monitor for extended pneumothorax and heamothorax
Keep the drainage system below the level of chest and tubes free of
kinks or any other obstruction.
Encourage coughing and deep breathing
Frequent position change to promote drainage and ventilation.
Do not milk or strip the tube without the order of the physician
Never clamp the tube without the order
If the chest tube is accidently pulled out, pinch the skin opening
together and apply an occlusive sterile dressing.
Cover the dressing with an overlapping pieces of 2 inch tape and call
the physician immediately.
When the tube is removed, the client is asked to take a deep breath
and hold it while the tube is removed. Apply dry sterile dressing or
petroleum gauze dressing or telfa dressing as per order.
Increasing the suction and emptying the bottles are not recommended
without the order.
A bottle of sterile water should be readily available at bedside.

15
VENTILATOR

Mechanical Ventilator
It is a positive +ve or –ve pressure breathing device that can maintain
ventilation and O2 delivery for a prolonged period
Indications:

Continuous decrease in PO2 (90-100)

An increase in PCO2 (35-45)
Persistent acidosis (PH less than 7.35)
Post thoracic or abdominal surgery
Drug overdose
Neuro muscular diseases (Gullen bary’s syndrome)
Inhalation injuries (Steam injuries)
Comatose patients
COPD
Shock
Mutisystem failure
Apnea which is not readily reversible
Snake poisoning

Types Of Ventilators

-ve pressure ventilator

+ve pressure ventilator

-ve pressure ventilator:

It exerts a negative pressure on the external chest or chest wall. It
decreases the intra thoracic pressure during inflation and allows air to
flow in to the lungs. Do not need intubation and it is adaptable to home

16
needs
Eg: Body wrap (pneumo wrap), Drinkes respirator tank (iron lung)
+ve pressure ventilators
It needs endo tracheal intubation or tracheostomy. It provides a passive
expiration

Types:
Pressure cycled
Time cycled
Volume cycled

Pressure cycled ventilators:

Ends inspiration when a preset pressure is reached. Tidal volume varies
Time cycled ventilators:
Terminates inspiration after a preset time. Respiratory rate is set. Used
in new borns and infants
Volume cycled ventilators:
Volume of air to be delivered with each respiration is preset.
Tidal volume: Wt in Kg × 10-15ml
Respiratory rate: 12-16mts
FIO2: 100% of O2 (concentration of O2 delivered)
Sensitivity setting: The patient should have to generate a –ve pressure
of greater than 2cm H2O as inspiratory force to trigger the ventilator

Modes:
Controlled Ventilation Mode: The machine completely controls
patient’s ventilation
Assist or controlled Mode: Patient triggers the machine. If the patient
fails to breath, the machine will deliver

17
SIMV (Synchronised Intermittent Mandatory Ventilator):
Spontaneous breath by patient, provide preset FIO2 and the number of
ventilator breaths
Inhalation exhalation rate is 1:3 or 1:2
BIPAP: Tight air breather mask; 100% FIO2
T Piece: One end with the patient, One end for atmospheric O2, One
end for FIO2. Patient is kept on it for 1 week. Extubate within 2 to 3 hrs
after the patient gets stabilized

Settings
When low pressure alarm beeps, it may be due to air leak
High pressure alarm may be due to increased secretions, airway
obstructions, broncho spasm, pulmonary edema, pneumothorax or
patient exhales when ventilator inhales

Sigh: The lungs are hyper inflated periodically to open the collapsed
alveoli. Sigh volume is 1.5 times the tidal volume. It has to be instilled at
1-3 times per hour
Nursing care:
Assess

 Vitals
 Evidence of skin colour (cyanosis, skin colour, peripheral refilling)
 Respiratory rate and pattern (Bilateral expansion)
 Neurological status (Reflexes, stimuli)
 Breath sounds (Rhales, wheezing- block; Crackles- Pulmonary
edema; Absence of breath sounds- Pneumothorax)
 Tidal volume
 Minute ventilation

18
  Minute volume (Tidal volume × respiratory rate)
 Suctioning needs
 Patient’s spontaneous respiratory effort
 Nutritional status
 Psychologic status (Confusion, altered sensorium)
 Cardiac function

Management

 Pain medication to relieve pain but it should not suppress

respiratory drive (Avoid Morphine)
 Frequent repositioning 2nd hrly
 Fluid balance to maintain adequate urine output of 40ml/hr
 Medications (Rhyles tube, IV, infusion pumps)
 Sterile techniques
 Chest physio (Percussion, vibration)
 ABG analysis 4th hrly
 Maintain cuff pressure under 25cm H2O every 8 hrs
 Buckling the ventilator: This is manifested when patient is
attempted to breath in or out during the inspiratory phase of
mechanical ventilator. It may be due to anxiety, hypoxia,
increased secretions, inadequate minute volume (6-8 l/mt) or
pulmonary edema.
Use muscle relaxants, tranquilizers, analgesics, paralyzing agents
(Vencuronium, pancuronium, Atracurium, Pavilon)
 Assess for Pneumothorax, Pulmonary infection
 Assess the patient first and ventilator second

19
20
MYOCARDIAL INFARCTION

Acute necrosis of heart muscle caused by interruption of O2 supply to

the area resulting in altered function and reduced cardiac output. It
occurs when myocardial tissue is abruptly and severely deprived of O2.
Ischemia can lead to necrosis of myocardial tissue, if blood flow is not
restored.

Etiology:
Deposition of fatty plaques along inner wall of coronary arteries leads
to inflammation.
Risk factors:
Atherosclerosis
CAD
Increased cholesterol level
Smoking
Hypertension
Obesity
Physical inactivity
Impaired glucose tolerance
Stress
Diagnostic studies:
Total CK level – rises within 3 hrs after the onset of chest pain and
peaks within 24hrs after damage and death of cardiac tissue.
CKMB Isoenzyme – rises in 4-6 hrs,peak elevation occurs12-24hrs after
the onset of chest pain and Level returns to normal after 48-72 hrs
Troponin level – rises within 3hrs and remains elevated up to 7 days

21
LDH – rises within 12-24hrs after MI, peaks between 40-72hrs and fall
to normal in 7 days
Serum levels of LDH1 rises higher than serum levels of LDH2
WBC Count increases
ECG – ST segment elevation and T wave inversion; hours to days after
MI, ST and T wave changes will return to normal but Q wave usually
remains permenant

Management:
Assess vitals
Obtain 12 lead ECG
O2 2-4L /nasal cannula
Semi fowlers position
Administer nitroglycerine and anti dysrhythmics as prescribed
Monitor signs of bleeding if the client is receiving thrombolytic therapy
which may be prescribed within first 6 hrs of the coronary event
Monitor complications related to MI such as Heart Failure, Pulmonary
edema, Cardiogenic shock, Thrombophlebitis, Pericarditis, mitral valve
insufficiency, Dressler’s syndrome( a combination of pericarditis,
pericardial effusion and pleural effusion which can occur several week
to month following MI)

ANGINA

Chest pain resulting from myocardial ischemia caused by inadequate

myocardial blood and O2 supply
Etiology:
Caused by an imbalance between O2 supply and demand
Causes include obstruction of coronary blood flow because of

22
atherosclerosis, coronary spasm and conditions which increase
myocardial O2 consumption such as exercise, smoking, physical exertion
etc.

Patterns of Angina:
Stable Angina(Exertional angina) occurs with activities that include
exertion or emotional stress and is relieved by rest or nitroglycerine. It
usually has a stable pattern of onset, duration, severity and relieving
factors.
Unstable Angina(Pre infarction angina) occurs with an unpredictable
degree of exertion or emotion and increases in occurrence, duration and
severity over time. Pain may not be relieved with nitroglycerine.
Varient Angina/Vasospastic Angina/Prinzmetal’s result from coronary
artery spasm. It is similar to classic angina but lasts longer. It may occur
even at rest.
Intractable Angina is a chronic angina that is irresponsive to
intervention
Pre infarction Angina: associated with acute coronary insufficiency
which
lasts for 10mts
Post infarction Angina: occurs after an MI

Assessment:

Pain
substernal crushing, squeezing pain which may radiates to shoulders,
arm, jaws, neck and back
usually lasts less than 15mts; however can last up to 15-20mts

23
relieved by nitro glycerin at rest
dyspnoea
pallor
sweating
palpitation
dizziness
faintness
hypertension

Diagnosis:

ECG: T wave inversion or ST depression during an episode of pain

Stress Test: chest pain or changes in the ECG or vital signs during the
test indicates ischemia
Cardiac enzymes: normal in angina

Implementation:

Immediate management
assess pain
provide bed rest
administer oxygen 3L per nasal cannula
administer nitro glycerin as prescribed to dilate the coronary artery
obtain 12 lead ECG
cardiac catheterization (PTCA)

24
HEART FAILURE

The inability of the heart to maintain circulation to meet the metabolic

needs of the body because of impaired pump capability (reduced
cardiac output)

Acute: occurs suddenly

Chronic: develops over time (DM, cardiac diseases)

Types of Heart failure

Right sided heart failure

Left sided heart failure

Assessment
Right sided heart failure:
Signs of Right sided Heart failure will be evident in the systemic
circulation
Pitting dependent edema in the feet, leg, sacrum and back
Ascitis from portal hypertension
Tenderness of right upper quadrant
Organomegaly
Anorexia
Nausea
Fatigue
Weight gain
Nocturnal diuresis
Left sided Heart Failure:
Signs of left sided Heart failure will be evident in pulmonary system
25
Cough which may become productive with frothy sputum
Dyspnea upon exertion
Orthopnoea
Paroxysmal nocturnal edema
Acute Pulmonary edema

Management:
Place the client in high fowlers position with the legs in a non
dependant position to reduce pulmonary congestion and relieve edema
Administer O2
Prepare for intubation and ventilator support
Suction as needed
Monitor vitals
Monitor Heart rate and signs of Dysrhythmias by using a cardiac
monitor
Assess for edema in dependant areas and in the sacral, lumbar and
posterior thigh region of the client in bed rest
Foleys Catheter as prescribed
Monitor I/O chart

CARDIOGENIC SHOCK

It is the failure of the heart to pump adequately, thereby reducing

cardiac output and compromising tissue perfusion
Necrosis of more than 40% of the left ventricle occurs.
The goal of treatment is to maintain tissue oxygenation and perfusion
and improve the pumping ability of the heart
Assessment

26
Hypotension (lower than 90/30mm Hg)
Oliguria
Cold, Clammy skin
Poor peripheral pulses
Tachycardia
Pulmonary congestion
Tachypnea
Disorientation, restlessness and confusion
Continuing chest discomfort

Intervention

Administer Morphine Sulphate

Administer diuretics and nitrates; assess BP continuously
Administer Vasopressors and positive inotropics
Administer oxygen
Monitor urine output
Monitor distal pulse
Monitor ABG
Prepare for mechanical ventilation
Prepare for PTCA or CABG

HYPERTESION

Persistent elevation of systemic BP above 140mm Hg and diastolic BP

90mm Hg
Types:
Primary/essential:
No known etiology
Risk factors:
27
Ageing
Family history
Obesity
Smoking
Stress
Secondary Hypertension:
Occurs as a result of other disorders and conditions such as cardio
vascular disorders, renal disorders, pregnancy etc.
Assessment:
Asymptomatic
Head ache
Visual disturbances
Dizziness
Chest pain
Tinnitus
Flushed face
Epitaxis
Management:
Goal to reduce BP and to prevent the extent of organ damage
Obtain BP two or more times of both arms
Family history of hypertension
Assess for visual changes of retinal damage
Medical management:
Diuretics, Beta blockers, Angiotensin converting enzyme inhibitors

HYPERTENSIVE CRISIS

28
Any clinical condition requiring any immediate reduction in the BP.
It is acute and life threatening condition
Death can be caused by stroke, renal failure and cardiac diseases
Assessment:
Head ache
Diastolic pressure above 120mmHg
Drowsiness
Confusion
Tachycardia
Tachypnea
Management:
Patent airway
Anti hypertensive medication
Nitropruside (diazoxide) direct acting vaso dialator
Monitor vitals and BP every 5 mts
Assess for hypotension during the administration of anti hypertensives

CORONARY ARTERY DISEASE

CAD is the narrowing or obstruction of one or more coronary arteries as

a result of atherosclerosis.
The disease causes decreased perfusion of myocardial tissue and
inadequate myocardial oxygen supply leading to hypertension, angina,
dysrhythmias, MI, heart failure and death.
The goal of treatment is to alter the atherosclerotic progression
Assessment

29
Possibly normal findings during asymptomatic periods
Chest pain
Palpitations
Dyspnea
Syncope
Cough or hemoptysis
Excessive fatigue

Diagnostic studies

ECG: ST depression and/or T wave inversion

CAG
Blood lipid levels: may be elevated

Intervention

Instruct the client regarding the purpose of diagnostic medical and

surgical procedures
Assist the client to set goals to promote lifestyle changes to reduce the
impact of risk factors
Instruct the client regarding a low calorie, low sodium, low cholesterol
and low fat diet with an increase in dietary fiber
Provide community resources to the client regarding exercise, smoking
cessation and stress reduction as appropriate
Surgical Intervention
PTCA
Laser angioplasty
Atherectomy
Vascular stent
CABG
30
Medical management
Nitrates to dilate coronary arteries
Calcium Channel blockers to dilate coronary arteries and reduce
vasospasm
Cholesterol lowering medications
Beta blockers

PACEMAKER

Instruct the client about the pacemaker, including the programmed rate
Instruct the client to notify the physician when the signs of battery
failure occur such as dizziness, weakness or fatigue, swelling of the
ankles or legs, chest pain or sudden shortness of breath
Instruct the client to report any fever, redness, swelling or drainage
from the insertion site
Keep a pacemaker identification card in the wallet and wear a medic
alert bracelet
Instruct the client in how to take pulse, to take the pulse daily, and to
maintain a dairy of pulse rates
Wear loose fitting clothing over the pulse generator site
Avoid contact sports
Inform all health care providers that a pacemaker has been inserted
Instruct the client to inform airport security because the pacemaker
may set off the security detector
Instruct the client that most electrical appliances can be used without
any interference with the functioning of the pacemaker; however advise
the client not to operate electrical appliances directly over the

31
pacemaker site
Instruct the client that if any unusual feelings occur when near any
electrical devices to move 5 to 10 feet away and check the pulse
Avoid transmitter towers and antitheft devices in stores
Emphasize the importance of follow up care
Use cell phones on the side opposite to the pacemaker

PERIPHERAL ARTERIAL DISEASE

A chronic disorder in which partial or total arterial occlusion deprives

the lower extremities of O2 and nutrients
Tissue damage occurs below the level of the arterial occlusion
Atherosclerosis is the common cause of PAD
Assessment:
Intermittent claudication
Rest Pain: numbness, burning or aching in the distal lower extremities
Lower back or buttock discomfort
Thickened toe nails
Cold and grey blue color skin in the lower extremities
Elevational pallor and dependent rubor in the extremities

Raynaud’s Disease

Vasospasm of the arteries and arterioles of the upper and lower

extremities
Vasospasm causes constriction of the cutaneous vessels
Attacks are intermittent and occur with exposure to cold or stress
Primarily affects fingers, toes, ears and cheeks
Assessment:
32
Blanching of the extremities followed by cyanosis during
vasoconstriction
Reddened tissues when vasospasm is relieved
Numbness, tingling and swelling and cold temperature of the affected
body part
Management:
Monitor pulse
Instruct the client regarding medication (vasodilators)
Identify and avoid precipitating factors such as cold and stress
Instruct the client to wear warm clothing

Buerger’s Disease (Thrombo Angitis Obliterans/TAO)

Occlusive disease of median and small arteries and veins

Distal upper and lower limbs are most affected
Intermittent claudication
Ischemic pain occurs at digits while at rest
Pain more severe at night
Cool, numbness & tingling sensation
Diminished pulses in the distal extremities
Management:
Stop smoking
Monitor pulse
Administer vasodialators as prescribed

33
Blood Disorders

SICKLE CELL DISEASE

Condition in which HgbA is completely or partially replaced by abnormal

sickle HgbS.
It is caused by inheritance of genes for a structurally abnormal portion
of the Hb chain
Insufficient O2 causes the cells to assume a sickle shape and the cells
become rigid and clumped together obstructing the capillary blood flow
Precipitating Factors:
Fever
Emotional and physical stress
Any condition that increases the body’s need for O2 and alters the
transport of O2 can result in Sickle cell crisis
Sickling response is reversible under conditions of adequate
oxygenation and hydration

Sickle cell Crisis

Acute exacerbation of sickle cell disease

This includes vaso occlusive crisis, splenic sequestration & aplastic crisis
Vaso occlusive crisis:
Stasis of blood occurs due to the clumping of cells in the micro
circulation. This results in ischemia and infarction
Signs:
Fever
34
Pain
Tissue engorgement
Arthralgia
Priapism
Hand and foot syndrome
Splenic sequestration:
It is a life threatening situation occurs due to the pooling of blood in the
spleen
Signs:
Anemia
Hypovolemia
Shock
Aplastic Crisis:
Diminished production and increased destruction of RBC
Prevention:
Avoid exposure to infection and maintain normal hydration

Implementation:
Oxygenation
Blood transfusion
Hydration
Pain management by Analgesics
IV NS
Comfortable positions to promote venous return; Avoid dependent
position
Elevate head of the bed not more than 30 degree
High calorie and high protein diet with folic acid supplement

35
Bed rest
Antibiotics

HEMOPHILIA

It is an ‘X’ linked recessive trait that is males inherit hemophilia from

mother and females inherit carrier status from father

Hemophilia A (classic hemophilia): due to the deficiency of Factor VIII

Hemophilia B (Christmas disease): deficiency of Factor IX
Assessment:
Abnormal bleeding
Joint bleeding
Pain
Tenderness
Swelling
Limited range of motion
Prolonged PTT
Normal BT, PT and platelet count
Implementation:
Factor VIII concentrate
Monitor clinical features
Immobilization to control bleeding
Elevation
Application of pressure/ice
Avoid contact sports (risk of injury)

IRON DEFICIENCY ANEMIA

36
Fe stores depletion
Causes:
Blood loss
Increased metabolic demands
GI mal absorption
Dietary inadequacy
S/S:
Pallor
Weakness
Fatigue
Irritability
Implementation:
Increase oral intake of Fe
Liver, nuts, dried fruits, beans, legumes, egg yolk, bread, cereals and
green leafy vegetables
Instruct the client about the side effects of Fe supplementation like
black stools, constipation, staining of teeth etc.

APLASTIC ANEMIA

Deficiency of circulating erythrocytes (RBC)

Causes:
Exposure to myeto toxic agents (bone marrow toxic)
Virus or Viral infections
Autoimmune disorders
Diagnosis:
Bone marrow aspiration (iliac crest, sternum)
Assessment:

37
Pancytopeania
Patechiae
Purpura
Pallor
Weakness
Tachycardia
Fatigue
Activity intolerance (Alternate period of rest and activity)
Intervention
Blood transfusion
Immono suppressive therapy – corticosteroids
Bone marrow transplantation
Administer Anti Lymphocytic Globulin and Anti thymocytic globulin.

THALACEAMIA

An Autosomal recessive disorder

Reduced production of one of the globulin chains
It is highest in mediteranian deserts
Assessment:
Severe Anemia
Pallor, fatigue and failure to thrive
Hepato splenomegaly
Microcytic hypochromic RBC
Frontal bossing
Maxillary prominence
Wide set eyes with flattened nose
Greenish yellow skin tone

38
Implementation
Goal of treatment is to maintain Hb level by blood transfusion
Bone marrow transplantation
Folic acid
Monitor for Fe overload
Administration of chelation therapy with Deferonamin (Disferal)
(antidote for Fe toxicity)
Genetic counseling

SLE (Systemic Lupus Erythematosis)

A chronic progressive systemic inflammatory disease that can cause

major organs and systems to fail. It is an auto immune disease. i.e. the
body is unable to recognize it’s own cells as a part of itself
It can affect collagenous tissue
It leads to necrosis and/or inflammation of blood vessels, lymph nodes,
GI tract, Pleura etc.
There is no cure for the disease.
Causes:
Unknown etiology although the disease is thought to be a defect in the
immunological mechanism or to have a genetic origin
Precipitating factors include medicine, stress, genetic factors, sunlight
and UV rays
Assessment:
Dry scaly raised rash on the face or upper body
Fever
Weakness, malaise and fatigue
Anorexia

39
Weight loss
Photosensitivity
Arthralgia
Erythema of the palms
Butterfly erythema of the face
Anemia
Increased ESR
Implementation:
Monitor skin integrity by using mild soap and ointments
Oral care
Fe, Folic acid and Vitamin Tablets
Administer topical and systemic corticosteroids (Treatment of choice)
NSAIDS (Brufen)
Hydrochloroquine (Plaquenil) to reduce inflammation
Emotional support
Supportive therapy

LEUKEMIA

Malignant exacerbation in the number of leukocytes usually at an

immature stage in the bone marrow.
Acute and chronic
Etiology:
Cause is unknown
Appears to involve gene damage of cells leading to the transformation
of cells from normal state to a malignant state.
Risk factors:
Genetic

40
Viral
Immunological and environmental factors
Exposure to radiation, chemicals and medication
Types:
Acute Lymphocytic Leukemia (ALL): mostly lymphoblast present in bone
marrow; age of onset is below 15
Acute Myelogenous Leukemia (AML): mostly myeloblasts are present in
bone marrow; age of onset is between 15-39 yrs
Chronic Myelogenous Leukemia (CML): mostly granulocytes are
present in bone marrow; age of onset is after 50 yrs
Chronic Lymphocytic Leukemia (CLL): mostly lymphocytes are present in
bone marrow; age of onset is after 50 yrs
Assessment:
Anorexia, fatigue, weakness, weight loss
Anemia, bleeding
Petechiae
Prolonged bleeding after minor abrasion or laceration
Increased temperature
Pallor, Dyspnea
Bone pain, joint swelling
Decreased Hb, platelet count and hematocrit levels
Infections
Intervention:
Strict aseptic precaution
Measures to control fatigue; provide adequate nutrition
Chemotherapy
Antibiotic, Antibacterial, Anti fungal and Anti viral medications

41
Psychological Support
Homecare measures

HODGKIN’S DISEASE (HODGKIN’S LYMPHOMA)

Malignancy of the lymph nodes that originated in a single lymph node

or a single chain of nodes.
Metastasis occurs to other lymph nodes, tonsils, spleen and bone
marrow and is characterized by the presence of Reed Sternberg cells in
nodes
Assessment:
Fever, malaise, fatigue and weakness
Night sweats
Anorexia and wt loss
Anemia, thrombocytopenia (decreased platelet count; high risk for
infection; check temperature daily)
Enlarged lymph nodes with cervical nodes most often affected
first(painless, movable and firm nodes or adenopathy in the
supraclavicular and cervical region)
Presence of Reed Sternberg cells in the nodes
Stages:
Stage 1: involvement of a single lymph node region or an extra
lymphatic organ or site
Stage 2: Involvement of two or more lymph node regions on the same
side of the diaphragm
Stage 3: Involvement of lymph node region on both sides of the
diaphragm

42
Stage 4: Diffuse or disseminated involvement of one or more extra
lymphatic organ with or without associated lymph node involvement
Implementation:
For stages 1 & 2 without mediasternal node involvement, the treatment
is extensive external radiation of the involved lymph node region
Chemo therapy
Complication:
Sterility in male client

MULTIPLE MYELOMA

A malignant proliferation of plasma cells and lumen within the bone

An excessive number of abnormal plasma cells invade the bone marrow;
develop in to lumen; ultimately destroy bones and invasion of lymph
nodes, spleen and liver occur
Abnormal plasma cells produce an abnormal antibody
Myeloma protein or Bence Jones protein found in blood and urine
Assessment:
Bone pain
Weakness & fatigue
Recurrent infections
Anemia
Bence Jones proteinuria & increased total serum protein level
Osteoporosis
Implementation:
Chemotherapy
Supportive care
Sign of bleeding

43
Monitor signs of Renal failure
Blood transfusion
Provide hazard free environment(osteoporosis fracture)
Analgesics
Antibiotics

44
Renal SYSTEM

45
Renal Calculi

Calculi are stones that can form anywhere in the urinary tract;
however the most frequent site is the kidneys.

Urolithiasis: formation of urinary calculi in the ureters

Nephrolithiasis: formation of calculi in renal parenchyma
Manifestations:
Pain
Obstruction
Tissue trauma
Secondary hemorrhage
Infection
If the obstruction is not removed, urinary stasis results in infection,
impairment of renal function on the side of the blockage,
hydronephrosis and irreversible kidney damage.
Causes:
Family History
Diet high in Ca, Vit.D, milk, protein, oxalate, purines or alkali
Obstruction and urinary stasis
Dehydration
Use of diuretics which can cause volume depletion
UTI and prolonged urinary catheterization
Immobilization
Hypercalcemia and hyperparathyroidism
Elevated uric acid level such as in gout
Assessment:
Renal colic, which orginates in the lumbar region and radiates around

46
the side and down to the testicles in men and to the bladder in women
Ureteral colic, which radiates toward the genitalia and thighs
Sharp severe pain of sudden onset
Dull aching pain in the kidney
Nausea and vomiting, pallor and diaphoresis during acute pain
Urinary frequency with alternating retention
Low grade fever
High numbers of RBC,WBC and bacteria in the urinalysis
Hematuria
Interventions:
Monitor vitals, especially temperature for the signs of infection
Monitor intake and output
Assess for fever, chills and infection
Monitor for nausea, vomiting and diarrhea
Encourage fluid intake up to 3000ml/day unless contraindicated
IV fluids if necessary
Strain all the urine for the presence of stones
Send stones to the lab for analysis
Provide warm bath and heat to the flank area
Administer analgesics in scheduled intervals and assess the client’s
response
Assist the client in relaxation techniques to relieve pain
Encourage ambulation
Turn and reposition immobilized clients
Diet specific to the stone component:
calcium phosphate stone-acid ash diet
calcium oxalate-acid ash diet

47
 struvite stones-acid ash diet, limit high phosphate food
uric acid stones-alkaline ash diet, less high purine food
cystine stones-alkaline ash diet
Prepare for surgical procedures if prescribed.

Benign prostatic Hypertrophy

BPH is a slow enlargement of the prostate gland with hypertrophy and

hyperplasia of the normal tissue. The enlargement causes narrowing of
the urethra and results in partial or complete obstruction.
Cause is unknown; commonly seen in males after 50 years

Assessment:
Urinary frequency and hesitancy
Changes in the size and force of urinary stream
Retention
Dribbling
Nocturia
Urinary stasis
UTI
Hematuria

Implementation:
Encourage fluids up to 2000-3000ml/day unless contraindicated
Prepare for bladder drainage through urinary catheterization for
distension
Avoid administering medication that cause urinary retention such as
anticolinergics, anti histamines and decongestants

48
Administer Finasteride (Finast 5 mg) as prescribed to shrink the
prostate gland and to improve the urine flow

Surgical Interventions:
Trans Urethral Resection of Prostate (TURP)
Retro pubic prostatectomy
Supra pubic prostatectomy
Perineal Prostatectomy

Nephrotic syndrome

A set of clinical manifestations arising from protein wasting caused by

diffuse glomerular damage
Assessment:
Proteinuria
Hematuria
Hypoalbuminemia
Hyperlipidemia
Edema (generalized periorbital that is most notable in the morning and
in dependent positions)
Anemia
Waxy pallor to the skin
Anorexia
Malaise
Irritability
Amenorrhea or abnormal mensus
Interventions:
Monitor vitals (Bp)

49
Monitor I/O
Bedrest if necessary if severe edema is present
Monitor daily weight
Measure abdominal girth or extremity size
Avoid trauma to the edematous tissues
provide a low to moderate Na and protein diet that is adequate in
carbohydrate and calories as prescribed to prevent worsening of
azotemia and fluid retention
Monitor S. Potassium level
Anti hypertensives, diuretics and lipid lowering agents
Corticosteroids and cytotoxic medications
Plasma volume expanders such as albumin, plasma and dextran to
increase the osmotic pressure
Anticoagulants as prescribed for clients who develop renal vein
thrombosis

Polycystic Kidney disease

A cystic formation and hypertrophy of the kidneys which leads to cystic

rupture, infection, formation of scar tissue and damaged nephrons
There is no specific treatment to arrest the progress of the destructive
cysts
The ultimate result of this disease is Renal failure
Types:
Infantile polycystic disease: An Inherited Autosomal Recessive trait that
results in the death of the infant within a few month
Adult Polycystic disease: AN autosomal dominant trait that manifests
between 30 and 40 yrs of age

50
Assessment:
Often asymptomatic during the ages of 30-40yrs
Flank, lumbar or abdominal pain that worsens with activity and is
relieved when lying
Fever and chills
UTI
Hematuria, proteinuria, pyuria
Calculi
Hypertension
Palpable abdominal masses and enlarged kidneys
Intervention:
Monitor for gross hematuria, which indicates cyst rupture
Provide bedrest if ruptured cyst and bleeding occur
Increase Na and H2O intake because Na loss rather than retention
occurs
Prepare the client for percutaneous cyst puncture for relief of
obstruction or for draining an abcess
Prevent and /or treat UTI
Prepare the client for dialysis or renal transplantation
Genetic counseling
Psychological support

Hydronephrosis

Distension of the renal pelvis and calices caused by an obstruction of

normal urine flow
The urine becomes trapped proximal to the obstruction
The causes include calculus, tumors, scar tissue, ureter obstruction, BPH

51
etc.
Assessment:
Hypertension
Head ache
Colicky or dull flank pain that radiates to the groin
Intervention:
Monitor vitals
Monitor for fluid and electrolyte imbalances, including dehydration
after the obstruction is relieved
Monitor for diuresis which can lead to fluid depletion
Monitor weight daily
Monitor urine for specific gravity, albumin and glucose levels
Fluid replacement
Prepare the client for insertion of nephrostomy tube or surgical
procedures to relieve the obstruction

Renal Failure

Loss of kidney function; it is acute and chronic

Symptoms are caused by retention of waste, retention of fluid and
inability of the kidney to regulate electrolytes
Pre renal cause:
Intra vascular volume depletion (hypovolemia)
Decreased cardiac output
Vascular failure secondary to vasodilatation and obstruction
Intra renal cause:
Tubular necrosis
Nephro toxicity

52
Alteration in the renal blood flow
Post renal cause:
Obstruction of the urine flow between kidney and urethral meatus
(hydro nephrosis)
Bladder neck obstruction

Acute Renal Failure

Sudden loss of kidney function caused by renal cell damage from

ischemia or toxic substances. Acute renal failure occurs abruptly and
can be reversible.
It leads to hypoperfusion cell death and decompensation of renal
function.
The prognosis depends up on the cause and condition of the client

Causes:
Infection
Renal artery occlusion
Dehydration
Diuretic therapy
Ischemia from hypovolemia
Heart failure
Septic shock/blood loss
Toxic substances such as medications particularly antibiotics

Phases:
Oliguric phase:
Duration lasts for 8-15 days; longest the duration, less chance for

53
recovery
Sudden drop in the urinary output; i.e. less than 400ml/day or 30ml/hr
Urine specific gravity 1.010-1.016
Anorexia
Nausea, vomiting
Hypertension
Decreased skin turgor
Tingling in the extremities
Pruritis
Drowsiness
Coma
edema
Cardiac disarrhythmia (hyperkalemia; more than 6)
Elevated BUN and creatinine
Signs of CHF
Signs of acidosis (PH less than 7.35, bicarbonate less than 22)
Diuretic phase:
Urinary output raises slowly and diuresis occurs 4-5L/day indicates the
recovery of the damaged nephrons
Hypotension
Hypokalemia
Hyponatremia
Hypovolemia
Tachycardia
Recovery Phase:
It is a slow process and may take 1-2 years.
Urinary volume is normal, increase in strength and increase in the level

54
of consciousness
If untreated the client can develop CRF.

Chronic Renal Failure

CRF is a slow, progressive, irreversible loss in kidney function.

It occurs in three stages and results in uremia or end stage renal
disease.
It affects all major body systems and requires dialysis or kidney
transplantation to maintain life
Hypervolemia can occur because of the kidney’s inability to excrete
sodium and water; hypovolemia can occur because of the kidney’s
inability to conserve Na and H2o

Stage 1 Stage 2 Stage 3

Renal function Begin to accumulate

Excessive accumulation
decreases
Oliguria
Kidneys are unable to
No accumulation of
maintain hemostasis
waste Edema

Healthier kidney Decreased

compensation responsiveness to
diuretics
Nocturia and polyuria

Ability of
concentrating urine

55
increases

Causes:
Recurrent ARF
Renal artery occlusion
Chronic Urinary Obstruction
Recurrent infections (nephritis)
Prolonged hypertension
Diabetes mellitus and other metabolic disorders
Auto immune disorders
Assessment:
Anorexia
Nausea and vomiting
Head ache
Weakness and fatigue
Hypertension
Confusion and lethargy
Kussumal Respiration
Diarrhea
Muscle cramps and numbness of the extremity
Decreased urine output

56
Proteinuria
Anemia
Azotemia
Fluid overload
Signs of HF
Presence of uremic frost
Intervention:
Monitor vitals (increased BP and pulse)
Monitor intake and output
Monitor weight daily (0.5-1 pound/day indicates fluid retention)
Monitor for acidosis and treat with Sodium bicarbonate as prescribed
Assess urine analysis for protein, hematuria and specific gravity
Assess level of consciousness
Assess signs of infection
Assess the risk of disarrhythmia since k+ level is above 6meq/L (peaked
T wave and widened QRS complex)
Monitor for fluid overload and assess the lungs for lung sound
Assess for anemia
Administer prescribed diet (low k+, low Ca)
Restrict Na+ intake
Daily fluid allowance can be 400ml-1000ml
Administer Sodium Polystrene sulphonate (cayesalate) to decrease k+
level
Be alert to nephrotoxic medications such as antibiotics
Prepare the patient for dialysis as prescribed

57
Hemodialysis

The diffusion of dissolved particles from one fluid compartment in to

another across semi permeable membrane. The client’s blood flows
through one fluid compartment and dialysate in another fluid
compartment.
Function:
Cleanse the blood from accumulated waste products
Remove excessive fluid
Maintains and restores the body’s buffers system
Maintain or restores the electrolytes level

Implementation:
Monitor vitals
Assess laboratory values before during and after the procedure
Assess the client for fluid overload prior to the procedure (Monitor wait
on same time everyday)
Assess the patency of blood access device(palpate thrill and auscultate
bruit)
Hold anti hypertensives and other medications that can affect BP prior
to the procedure
Hold the medication that could be dialyzed off such as water soluble
vitamins (Vit.B12) and certain antibiotics
Provide adequate nutrition

Complication:
Disequilibrium syndrome:
A rapid change in composition of extra cellular fluid occurs during
dialysis. i.e. solutes are removed from the blood faster than CSF and

58
brain; fluid is pulled in to the brain causing cerebral edema.
Dialysis encephalopathy:
An aluminium toxicity that occurs as a result of aluminium in the water
source used in the diazolate and an ingestion of aluminium containing
antacids (phosphate binders)
Administer Aluminium chelating agents(desferrioxamine) as prescribed
so that aluminium is freed up and dialized from the body.

Peritoneal Dialysis

The peritoneum is the dialyzing membrane and the substitute

for kidney function for kidney failure works on the principle of
diffusion and osmosis and dialysis occurs through the transfer of
fluid and solutes from the blood stream through the peritoneum.
The peritoneal membrane is large and porus allowing solutes and
fluid to move via an osmotic gradient from an area of high
concentration in the body to an area of low concentration in the
dialyzing fluid.

Types:
Continuous Ambulatory PD
Automated PD which requires a peritoneal cycling machine

Description:
One infusion (inflow), dwell and out flow is one exchange.
Inflow: The infusion of 1-2L of dialysate as prescribed is infused by
gravity in to the peritoneal space which usually takes
approximately 10-20 mts
Dwell Time: The amount of time that the dialysate solution
remains in the peritoneal cavity as prescribed by the physician (40
59
 mts)
Out flow: Fluid drain out of the body by gravity in to the drainage
bag which usually takes 20 mts

Implementation:
Monitor vitals
Monitor for respiratory distress, pain and discomfort
Monitor for pulmonary edema
Monitor for hypotension and hypertension
Assess the catheter site dressing for wetness or bleeding
Monitor dwell time as prescribed by the physician and initiate out
flow because it increases the risk for hyperglycemia
Turn the client from side to side or make the client sit upright if the
flow is slow to start
Monitor the out flow for colour and clarity
Monitor Intake and output accurately; if the out flow is less than
that of the in flow, the difference is equal to the amount absorbed
or retained in the client during dialysis and it should be considered
as intake

Complications:
Peritonitis
Abdominal Pain
Insufficient out flow
Leakage around the catheter site

Cancer of Bladder

60
 Papillomatus growth in the bladder urothelium that undergoes
malignant changes and infiltrate bladder wall.

Pre disposing factors:

Smoking
Exposure to industrial chemicals
Exposure to radiation

Common sites of metastasis include liver, bones and lungs. As the

tumour progresses, it can extend to the rectum, vagina and other
pelvic soft tissues.

Assessment:
Gross painless Hematuria
Frequency, urgency and disuria
Clot induced obstruction
Bladder biopsy confirms the diagnosis

Management:
Radiation
Chemotherapy – Intra vesical instillation of alkalating
chemotherapeutic agents in to the bladder. Agents include
Mutamycin, Doxorubilin and cyclo phosphamide

Surgical Management:
1. Partial Cystectomy for early tumours and for clients who
cannot tolerate radical cystectomy. CBD post operatively is
necessary. Urethral and suprapubic catheter is placed. Suprapubic
catheter is left in place for 2 weeks until healing occurs.

61
 2. Cystectomy and urinary diversion: Removal of bladder and
urethra in woman and bladder, urethra, prostate and seminal
vesicles in man.
Ileal conduct/ Uretero ileostomy/ Bricker’s Procedure
Kock’s pouch: A continent internal ileal reservoir is created from
the segment of ileum and ascending colon.
Creation of neo bladder: The client empties the neo bladder by
relaxing the external spincture and creating an abdominal
pressure or by intermittent self catheterization.
3. Ureterostomy
4. Vesicostomy

Management:
Bowel preparation includes clear liquid diet, laxatives and enema
Antibiotics to lower the bacteria in the bowel (neomycin)
Encourage the client to express the feeling about stoma creation
Post Op care:
Check vitals
Assess incision site
Assess stoma which should be moist and red in color for early one
hour
If the stoma appears dark and dusky in first 24 hours, notify the
physician
If urinary output is less than 30ml/hr, notify the physician
Note for Hematuria, shock, hemorrhage, thrombo phlebitis and
lower extremity lymph edema.
Monitor for the PH of urine as high PH of urine causes skin irritation
Instruct client regarding UTI and renal calculi

62
NEPHRO BLASTOMA (WILM’S TUMOUR)

Tumour of the kidney that may be present unilaterally or bilaterally

sometimes with the metastasis to the other organs
Peak incidence is at 3 yrs of age
Occurance is associated with genetic inheritance and with several
congenital anomalies
Assessment:
Swelling or mass in the abdomen characterized by non tender confined
to one side and deep within the flank
Urinary retention
Anemia
Pallor, Anorexia
Hypertension
Weight loss
Fever
Syptoms of lung involvement
Intervention:
Monitor vitals; particularly BP and temperature
Place a sign at the bed side “ Do not palpate the abdomen”
Monitor for the sign of hemorrhage and infection
Monitor I/O
Monitor for abdominal distension; indicates bleeding
Monitor for bowel sounds and other signs of GI activity because of the
risk for intestinal obstruction

63
GASTROINTESTINAL SYSTEM

64
GASTRO ESOPHAGEAL REFLUX DISEASE

GER is the back flow of the gastric and duodenal contents in to the
esophagus. The reflux is caused by the incompetent lower esophageal
sphincter, pyloric stenosis or a motility disorder
Symptoms may mimic those of a heart attack
Assessment:
Pyrosis
Dyspepsia
Regurgitation
Pain and difficulty with swallowing
Hyper salivation
Intervention:
Instruct the client to avoid factors that decrease lower esophageal
sphincter pressure or cause esophageal irritation
Instruct the client to eat a low fat, high fiber diet and to avoid caffeine,
tobacco & carbonated beverages
Avoid eating and drinking 2 hours before bed time
Avoid wearing tight clothes
Elevate the head of the bed 6-8 inches
Avoid the use of anti cholinergic which delay stomach emptying
Instruct the client regarding the administration of prokinetic medication
which accelerates stomach emptying
Surgical Intervention: Fundoplication
Wrapping a portion of the gastric fundus around the sphincter area
of the esophagus. It is a laparoscopic procedure

65
PEPTIC ULCER

It is the ulceration in the mucosal wall of the stomach pylorus,

duodenum or esophagus in portions that are accessible to gastric
secretions
Ulcer may be duodenal or esophageal but the most common is peptic or
gastric ulcer
Gastric ulcers involve the ulceration of mucosal lining that extends to
the sub mucosal layer of stomach
Pre disposing factors
Stress
Smoking
Corticosteroids
NSAIDS
Alcohol
Family history
Infection with H pyloric (Helicobacter pyloric)
Complications
Hemorrhage
Perforation
Pyloric obstruction
Assessment
Sharp pain in or on the left side of the mid epigastric region 1-2 hrs
after eating
Hemetemesis
Nausea and vomiting
Duodenal Ulcer
Burning pain in the mid epigastric area 2-4 hrs after eating and during

66
night
The pain is often relieved by eating
Melena
Implementation
Small, frequent and bland diet during active phase
H2 receptor antagonist (Histamine/Reglant) which reduces the HCL
production
Antacids neutralize gastric secretions
Anti cholinergics to decrease the gastric mobility
prostaglandin acts as a protection and antisecretory actions
Surgical Management
Total gastrectomy: Removal of stomach, duodenum attached to
jejunum
Vagotomy: excision of the vagus nerve to eliminate vagus impulses that
stimulate HCL in the stomach
Billroth 1: Partial gastrectomy/gastro duodenostomy; remaining
segment is anastamosed to the duodenum
Billroth 2: Gastro jejunostomy; partial gastrectomy with the remaining
portion anastamosed to jejunum
Pyloroplasty: Enlargement of the pylorus to prevent or decrease pyloric
obstruction and thereby enhancing gastric emptying
Surgical complication
Dumping syndrome: rapid emptying of the gastric contents in to the
small intestine. It occurs following gastric resection which subsides in 6-
12 months.
Assessment:
Symptoms occur 30mts after eating

67
Nausea, vomiting
Feeling of abdominal distension
Abdominal cramping
Diarrhea
Palpitation and tachycardia
Perspiration
Implementation:
To prevent dumping syndrome, eat high protein low carbohydrate diet;
small meals and avoid consuming fluid with meals
Avoid sugar and salt
Lay down after meals

ULCERATIVE COLITIS

Ulcerative and inflammatory disease of the bowel that results in the

poor absorption of nutrients
Colitis begins in rectum and spread to cecum. The colon becomes
edematous and may develop bleeding lesions and ulcers. These ulcers
may lead to perforation; scar tissue develops; causes loss of elasticity
and loss of ability to absorb nutrients
Ulcerative colitis results in vascular congestion, hemorrhage, edema
and ulceration
Assessment:
Anorexia
Wt loss
Malaise
Abdominal tenderness

68
Severe diarrhea
Anemia
Vitamin K deficiency
Surgical Management
Creating an ostomy
Ileostomy is a surgical creation of opening in to the ileum or small
intestine that allows the drainage of fecal matter from ileum to outside
of the body
Colostomy is a surgical creation of opening that allows drainage of fecal
matter from the colon
Kock’s ileostomy is an intra abdominal pouch that stores the feces and
is constructed from the terminal ileum. The pouch is connected to the
stoma with a nipple like valve. The stoma is flushed in skin
Intervention
Maintain NPO status
Administer fluid and electrolytes IV or TPN as prescribed
Restrict the client’s activity to reduce intestinal activity
Monitor for bowel sounds and for abdominal tenderness
Administer bulk forming agents
Instruct to avoid gas forming agents
Avoid smoking

CROHN’S DISEASE

It is an inflammatory disease that can occur anywhere in the GI tract

but most often affects the terminal ileum and lead to thickening and
scaring, narrowed lumen, fistulas, ulceration and abscess.
Assessment

69
Fever
Cramp like colicky pain after meal
Diarrhea; may contain mucus and pus
Abdominal distension
Anorexia, nausea and vomiting
Wt loss
Anemia
Dehydration
Intervention
Care is similar to that of clients with ulcerative colitis. However, surgery
should be avoided as much as possible because of the recurrence of the
disease process in the same region is likely to occur
Lying supine with the legs straight should be avoided

DIVERTICULITIS/DIVERTICULOSIS

It is an out pouching or herniation of an intestinal mucosa. The disorder

can occur at any part of the intestine but the most common site is the
Sigmoid colon.
Diverticulitis is the inflammation of one or more diverticula that results
when the diverticulum is perforated. A perforated diverticulum can
progress in to intra abdominal perforation with generalized peritonitis
Assessment
Left lower quadrant abdominal pain that increases with coughing,
straining or lifting
Increased temperature
Flatulence and cramp like pain
Abdominal distension

70
Palpable tender rectal mass
Blood in stool
Intervention
Bed rest during the acute phase
NPO in active phase
Antibiotics (Metrogyl, Neomycin[prophylactic])
Analgesics
Anti cholinergics to delay the intestinal motility and to reduce bowel
spasm
Monitor for perforation(rigid broad like abdomen) and hemorrhage
Increase fluid intake
Small frequent diet
Avoid high fiber food
Gradually introduce high fiber diet when the inflammation subsides.

CHOLECYSTITIS
Inflammation of the gall bladder that may occur as an acute or chronic
process
Acute inflammation is associated with gall stones or cholelithiasis
Chronic cholelithiasis results when inefficient bile emptying and gall
bladder muscle wall disease cause a fibrotic and contracted gall bladder
Acalculous cholecystitis occurs in the absence of gall stones and is
caused by bacterial invasion through lymphatic or vascular system
Assessment
Nausea, vomiting
Indigestion

71
Belching
Flatulence
Epigastric pain that radiates to the scapula 2-4 hrs after eating fatty
foods and may persist for 4-6 hrs
Pain localized in right upper quadrant
Rigidity, rebound tenderness
Mass palpated in rt upper quadrant
Murphy’s sign
Elevated temperature
Tachycardia
Signs of dehydration
Biliary obstruction: Jaundice, dark orange and foamy urine, steatorrhea
and clay coloured feces and pruritis
Intervention
Maintain NPO status during nausea and vomiting episodes
Maintain NG decompression as prescribed for vomiting
Administer Antiemitics
Administer analgesics, antispasmodics
Instruct the client with chronic cholecystitis to eat small, low fat meals;
avoid gas forming food
Prepare for surgical and non surgical procedures as prescribed
Surgical intervention
Cholecystectomy: removal of gall bladder
Choledocholithotomy: requires incision in to the common bile duct to
remove the stone
Post op intervention
Monitor for respiratory complications caused by pain at the incisional

72
site
Encourage coughing and deep breathing
Encourage early ambulation
Instruct the client about splinting the abdomen to prevent discomfort
during coughing
Antiemitics
Analgesics
NPO and NG suction as prescribed
Advance diet from clear liquids to solids as tolerated
Monitor drainage from T tube

PANCREATITIS

Acute or chronic inflammation of the pancreas with associated escape

of pancreatic enzymes in to surrounding tissue
Acute Pancreatitis is the sudden or recurrent attacks
Chronic Pancreatitis is the continuous inflammation of pancreas or scar
tissue
Precipitating factors
Trauma
Use of alcohol
Biliary tract disease
viral or bacterial disease
Hyperlipidemia
Hypocalcaemia
Cholelithiasis
Hyperparathyroidism
Ischemic vascular disease

73
Peptic ulcer
Assessment
Abdominal pain at the mid epigastric or left upper quadrant radiating to
the back
pain aggravated by fatty meals, alcohol or lying in supine position
Abdominal tenderness
Nausea and vomiting
Wt loss
Cullen’s sign (discolouration of the abdomen and periumbilical area)
Turner’s sign (bluish discolouration on the flanks)
Absent or decreased bowel sounds
Elevated WBC, glucose, bilirubin, alkaline,phosphatase, urinary amylase
etc.
Increased lipase & amylase
Implementation
NPO
Hydration with IV fluids
TPN
NG tube to reduce gastric destruction and suppress pancreatic secretion
Administer Mepiridine Hydrochloride
Administer Antacids, histamine receptor antagonists & Anticholenergics
Avoid alcohol
Notify clay coloured stool or dark coloured urine
Chronic pancreatitis
Assessment
Abdominal Pain and tenderness
Left upper quadrant mass

74
Steatorrhea
Foul smelling stool
Wt loss
Muscle wasting
Jaundice
S/S of DM
Implementation
Restrict Dietary fat and protein
Avoid heavy meals and alcohol
Supplemental preperations, vitamins and minerals
Administer pancreatic enzymes, insulin or oral hypoglycemic
medications(stimulates pancreas to secrete insulin to treat DM)

CIRRHOSIS

It is a chronic progressive disease of the liver characterized by diffused

damage to cell with fibrosis and nodular regeneration
Repeated destruction of hepatic cells causes the formation of scar tissue
Complications:
Portal hypertension: A persistent increase in the pressure within the
portal vein that develops as a result of obstruction to the blood flow
Ascitis: It is the accumulation of fluid within the peritoneal cavity that
results in the venous congestion of hepatic capillaries. Capillary
congestion leads to plasma leaking directly from liver surface and portal
vein.
Bleeding esophageal varices: Fragile thin walled distended esophageal

75
vein that become irritated and ruptured
Types:

Laennec’s cirrhosis/ Alcohol induced/ Nutritional/ Portal:

Cellular necrosis causes eventual wide spread scar tissue with
fibrotic infiltration of the liver.
Post necrotic cirrhosis:
occurs after massive liver necrosis as result of complication of acute
viral hepatitis or exposure to Hepato toxins. Scar tissue causes
destruction of the liver lobules and the entire lobe
Biliary cirrhosis:
Cirrhosis develops from chronic biliary obstruction. Bile stasis and
inflammation result in severe obstruction and jaundice
Cardiac cirrhosis:
Associated with severe right sided CHF results in enlarged
edematous congested liver and liver becomes anoxic resulting in liver
cell necrosis and fibrosis
Hepato renal syndrome:
It is a progressive renal failure associated with hepatic failure
characterized by sudden decrease in urinary output, elevated BUN and
creatinine & decreased urine osmolarity
Assessment:
Anorexia, wt loss
Early morning nausea and hemetemesis
Dyspepsia
Flatulence and changes in bowel habits
Emanciation
Fatigue and jaundice

76
Abdominal pain and tenderness
Ascitis
Peripheral edema
Dry skin and rashes
Ecchymosis and Patechiae
Spider angiomas on the nose, cheek, upper thorax and chest
Hepatomegaly
Protruded umbilicus
Dialated abdominal veins
Fetor hepaticus (fruity musky ordour in breath in chronic liver disease)
Astrixis (course tremer characterized by rapid non rhythmic extension
and flexion in the wrist and fingers)
Delirium
Implementation:
Elevate the head of the bed
High protein diet with Vitamin B complex, A, C, K, folic acid and
thiamine
(Avoid protein in case of Hepato encephalopathy)
Restrict Na+ and fluid intake
Initiate enteral feeding or TPN
Administer diuretics
Monitor I/O, electrolyte balance, Daily Wt and abdominal girth
Monitor yellowish discolouration of skin, LOC
Gastric intubation
Administer blood products
Administer low sodium Antacids
Monitor coagulation factors if needed

77
Administer lactulose to decrease PH of bowel
Administer Neomycin to increase protein synthesis by bacteria and it
decreases the production of ammonia
Avoid medications such as narcotics, sedatives and barbiturates
Restrict alcohol intake
Paracentesis to remove ascetic fluid
Surgical shunting procedure

TPN (Total Parental Nutrition)

It supplies necessary nutrients through veins such as carbohydrates in

the form of Dextrose, fats in simple emulcified form, proteins as
aminoacids, vitamins, minerals and H2O
Indication
GI Tract dysfunction
Non functional GIT
Multiple GI surgeries
Trauma
Intolerance
Obstruction
Need rest for healing
AIDS
Cancer
Malnutrition
Chemotherapy etc.
Components
Carbohydrates: Glucose/Dextrose

78
 5% Dextrose for peripheral parental nutrition
50-70% of glucose through central line
It provides 60-70% of total calories

Amino acids: It provides 3-15% of amino acids

Fats: 30% of the caloric needs
Vitamins
Minerals and trace elements
Water
Electrolytes
Insulin may be added to control glucose level
Heparin may be added to the fibrinous clots at the catheter tip
Intravenous site
Central vein
Internal jugular/sub clavian
Peripherally inserted central catheter (PICC)
Tunneled catheter
Implanted vascular access device
Peripheral line
Complications
Air embolism: Heart murmer, Dyspnea, hypotension, rapid & week
pulse, respiratory distress, chest pain
Pneumothorax: Chest & shoulder pain, sudden shortness of breath,
tachycardia, absence of breath sounds on affected side
Infection: High concentration of glucose increases the bacterial growth
Fever, chills, errhythema, drainage at the insertion site,
increased WBC, septic shock
Fluid overload: Bounding pulse, jugular vein distension, head ache,

79
hypertension, crackles in lungs on auscultation, wt gain more than
desired
Hyperglycemia: Excessive thirst, dieresis, fatigue, restlessness,
confusion, weekness, kusumal’s respiration & coma when it is severe
Hypoglycemia: Diaphoresis, shakeness, anxious, hunger
Implementation
For pneumothorax: confirm the position with X ray
Instruct the client in Vulsulva manure for tube and
cap changes
For Infection: Aseptic techniques
Assess IV site for redness, swelling, tenderness and
discharge
Change TPN solution every 12-24hrs
IV site dressing every 48hrs
To prevent fluid overload: Use electronic infusion device
Daily Wt monitoring
Monitor Intake and output
Check the TPN solution colour
Prevent infection and solution compactability
Monitor PTT,PT for clients receiving anti coagulants
Monitor electrolytes, albumin, LFT & RFT
In severely malnourished clients monitor for Refeeding syndrome( Rapid
drop in MG, K+,Ph serum level)
TPN stored in fridge to be administrated within 24hrs from the time it is
prepared
Do not use IV filter because fat emulsion particles are too large
Infuse initially at 1ml/mt

80
Monitor LFT, S. Lipids
Adverse reaction to lipids: Chills, fever, flushing, diaphoresis, Dyspnea,
cyanosis , chest and back pain, nausea & vomiting, head ache, pressure
over the eyes, vertigo, sleepiness & thrombophlebitis

**********************************************************

81
Endocrine system

Diabetes Insipidus

A hypo secretion of ADH or deficiency of vasopressin results in failure of

the tubular re absorption of water in the kidney
Assessment
Polyuria 4-24L/day
Polydipsia
Dehydration
Decreased skin turgor
Dry mucous membrane
Inability to concentrate urine
Urine specific gravity 1.006 or less
Fatigue
Muscle pain and weakness
Head ache
Postural hypotension
Tachycardia
Implementation
Monitor vitals
Neurological and cardio vascular status
Provide safe environment
Monitor electrolyte value for the sign of dehydration
Monitor intake/output
Monitor Wt
Specific gravity of urine

82
Adequate fluid intake
Avoid food and liquids with diuretic action (coffee, barley water)
Administer chlor propamide(diabenese), clofibrate
Administer vasopressin tannate (Pittressin), Desmopressin acetate,
lepressin etc.

Syndrome of inappropriate Antidiuretic Hormone (SIADH)

A disorder in which a continuous release of ADH occurs

Results in water intoxication
Assessment
Signs of fluid volume overload
Changes in LOC & mental status
Wt gain
Hypertension
Tachycardia
Anorexia
Nausea & Vomiting
Hyponatremia
Implementation
Monitor vitals, cardiac and neurological status
Monitor I/O, daily Wt,Electrolyte level
Provide safe environment
Fluid restriction
Administer diuretics & IV fluids
Administer Demeclocyline

83
Addison’s disease

Hyposecretion of adrenal cortex hormones (gluco corticoids & mineralo

corticoids)
Assessment
Lethargy
Fatigue
Muscle weakness
GI disturbances
Wt loss
Menstrual changes
Hypoglycemia
Hyperkalemia
Postural Hypotension
Dehydration
Emotional disturbances
Implementation
Monitor vitals, Wt, I/O, Blood glucose, K+ levels
Administer Glucocorticoid or mineralo corticoid medications
Avoid individuals with infection, stress, strenuous exercise & over the
counter medications
Need for lifelong glucocorticoid therapy
Addisonian Crisis
A life threatening disorder caused by acute adrenal insufficiency
Precipitated by stress, infection, trauma or surgery
Can cause Hyponatremia, Hyperkalemia, hypoglycemia and shock
Assessment
Severe abdominal, leg and lower back pain

84
Severe head ache
Generalized weakness
Irritability and confusion
Severe hypotension, shock
Implementation
Administer Hydrocortisone sodium Succinate (Solu-cortef)
IV Glucocorticoids
Following resolution of crisis, administer oral gluco and mineralo
corticoids
Monitor Vitals, neurological status, I/O, Lab values(Na+, K+, RBS)
Administer IV fluids
Protect from infection

Cushing’s syndrome

Resulting from hyper secretion of glucocorticoids from adrenal cortex

Caused by increased pituitary secretions of ACTH, a pituitary adenoma
or an adrenal adenoma
Assessment
Trunkal obesity with then extremities
Moon face, buffalo hump
Supraclavicular fat pads
Generalized muscle wasting and weakness
Fragile skin that easily bruises
Reddish purple stripes on abdomen and upper thighs
Hirsutism
Hypertension
Increased blood glucose, Na+, WBC

85
Decreased Ca, K+ Levels
Implementation
Monitor vitals, I/O, Wt, Lab values (blood glucose, WBC, Na+,K+, Ca)
Good skin Care
Administer Amino glutethimide (Elipten, cytadren), chemotherapeutic
agents
Radiation
Hypophysectomy
Adrenalectomy.

Pheochromo cytoma

A catecholamine(epinephrine & nor epinephrine)producing tumour

usually found in the adrenal gland and may also be in the abdomen
Hyper secretion of the hormones of the adrenal
medulla(Aldosterone)and excess amount of epinephrine & nor
epinephrine.
It is typically a benign tumour but can be malignant
Surgical excision of adrenal gland or symptomatic treatment
Complications
Hypertensive retinopathy
Nephropathy
Myocarditis
CHF
Increased platelet aggregation
CVA
Death due to shock, CVA, renal failure, dysarrhythmia or dissective
aortic aneurism

86
Assessment
Hypertension that is resistant to treatment with drugs
Severe head ache (occipital)
Palpitation
Profuse diaphoresis
Flushing
Pain in chest or abdomen with nausea and vomiting
Heat intolerance
Wt loss
Tremors
Hyperglycemia
Glycosuria
Implementation
Monitor vitals
Monitor for Hypertensive crisis
Avoid alcohol, caffeine & beverages(vasoconstriction)
Change position slowly
Keep Phentalo Amine(Regitine) at bedside for hypertensive crisis
Administer Alpha Adrenergic blocking agent, Phenoxy benzamine to
reduce BP
Monitor blood glucose, urine for glucose and acetone
Promote a non stressful environment
Diet high in calories, vitamins and minerals
Surgical management
Adrenalectomy: surgical removal of adrenal gland; it may be bilateral
Incase of bilateral Adrenalectomy, lifelong glucocorticoid therapy is
needed

87
Incase of Unilateral Adrenalectomy, temporary replacement for 2yrs is
needed
Catacholamine level may drop as a result of surgery which leads to CV
collapse, hypotension and shock
Hemorrhage may occur due to the high vascularity of the adrenal gland
Preoperative intervention:
Assess for hyperglycemia
Administer glucocorticoids
Protect from infection
Post operative intervention:
Monitor I/O, vitals(hypertension immediately after surgery), daily Wt,
electrolytes
Administer Mepiridine (Give it in caution as it causes hypotension)
Instruct the importance of glucocorticoid therapy after surgery

Diabetic Mellitus

It is a chronic disorder of impaired glucose tolerance and carbohydrates,

proteins and lipid metabolism caused by deficiency in insulin. It results
in hyperglycemia.
Assessment
Polyuria
Polydypsia
Polyphagia
Hyperglycemia
Wt loss
Blurred vision
Delayed wound healing

88
Vaginal Infection
Weakness and parasthesias
Signs of inadequate circulation to the feet
Intervention
Diet: Total number of calories is individualized on the basis of current or
reduced Wt and the presence of other existing health problems
Exercise: It lowers blood glucose level and decreases cardio vascular risk
Exercise improves circulation. It decreases total cholesterol and
triglyceride level
Instruct the client to monitor the blood glucose prior to exercise.
If the client plans to participate in extended periods of exercise, blood
glucose level should be checked before during and after exercise
Instruct the client to take carbohydrate snacks with protein to prevent
hypoglycemia
Oral hypoglycemic medications: It is prescribed for the client with Type
2 DM
Assess vitals and blood glucose level
Alcohol, Aspirin & sulphonamides, oral contraceptives and MAOI(Mono
Amine Oxydase Inhibitors) increases hypoglycemic effect
Instruct the client not to ingest alcohol with sulphonamides
Insulin: Used in the treatment of Type 1 & Type 2 DM where diet and wt
control therapy have failed to maintain satisfactory blood glucose level
Instruct the client to recognize symptoms of hypo and hyper glycemia

89
 Types Of Insulin
Type Onset Peak/Hrs Duration/Hrs
Rapid Acting
1/2 -1
Lispro ( Humalog) 15 mts 1/2Hrs 4 - 5 Hrs
Insulin Aspart (Novolog) 5 - 10 mts 1 - 3 Hrs 3 - 5 Hrs
Short Acting
Regular(Humalin R/Novolin
R) 1/2 - 1 Hr 2 - 4 Hrs 5 -7 Hrs
Intermediate Acting
NPH(Humalin N/Novolin N) 1 - 2 Hrs 6 - 14 Hrs 24 Hrs
Long Acting Insulin
Ultralent (Humalin U) 6 Hrs 18 - 24 Hrs 36 Hrs
Insulin Glarglene(Lantus) 24 Hrs
Premixed Insulin
Humalin 70/30 (NPH/R) 1/2 - 1 Hr 2 - 12 Hrs 18 - 24 Hrs
Humalin 50/50 (NPH/R) 1/2 Hr 3 - 5 Hrs 24 Hrs
75%Lipro protamine&25% 10 - 15
Lispro mts 1 - 6 Hrs 24 Hrs

To prevent dosage error, be certain that a match between the insulin

concentration noted on the vial and calibrations of units on the insulin
syringe
The usual concentration is 100U/ml
Most insulin syringes have 27 – 29 gauge needle that is about half inch
long
Before use, roll the insulin bottle to ensure that the insulin and the
ingredients mixed well; avoid shaking the vial that forms bubbles
Mixture of insulin in a prefilled syringe should be kept in the refrigerator
where it will be stable for at least 1 week

90
Prefilled syringes should be kept flat or with the needle in an upright
position to avoid clogging of the needle
Inject the air in to the insulin bottle, vaccum make it difficult to draw the
insulin
When mixing insulin, draw the regular insulin first because regular
insulin can mix with any other type of insulin
Administer mixed dose of insulin within 5 – 10mts after loading
Avoid exposing insulin to extreme temperature
It should not be frozen or kept in direct sunlight

Complications of Insulin Therapy

Local Allergic reactions:

Redness, swelling, tenderness and formation of wheel at the injection
site
Anti Histamines should be taken 1Hr prior to administration; cleanse the
skin with Alcohol swab before injection
Insulin lipodystrophy:
Lipoatrophy: Loss of subcutaneous fat
Lipohypertrophy: Development of fibro fatty mass at the injection site
caused by the repeated use of injection site
Instruct the client to rotate the site
Insulin Resistance:
The client taking insulin develops immune antibodies and thereby
decreases the insulin available for the use of the body
Use prednisolone to block the production of antibodies
Dawn Phenomenon:
It results from the nocturnal release of growth hormone which may

91
cause the blood glucose to begin to rise about 3am
Evening dose of intermediate acting insulin at 10pm
Somogyi Phenomenon:
Normal or elevated blood glucose levels are present at bedtime;
hypoglycemia occurs at 2 to 3am, which causes an increase in the
production of counter regulatory hormones. By 7am, in response to the
counter regulatory hormones, the blood glucose rebounds significantly
to the hyperglycemic range.
Decrease the evening dose of intermediate acting insulin or increase the
bed time snack

Complications of DM

Hypoglycemia:

Blood sugar level falls to less than 50 – 60 mg/dl

It may be caused by too much of insulin or oral hypoglycemic agents,
too little food or excessive activity
Assessment: Sweating, Tachycardia, Palpitation, Tremer, Nervousness,
Hunger and Head ache
Implementation:
Carry some form of fast acting simple carbohydrate

Diabetic Ketoacidosis (DKA):

It is a life threatening complication of DM that develops when a severe

insulin deficiency occurs (more than 300)
Assessment: Hyperglycemia, Dehydration, Ketosis and Acidosis
Blood glucose vary from 300 – 800mg/dl
Low S.Bicarbonate & reduced PH

92
 Low NA+ & K+
Implementation:
Use Regular insulin only
A dose of 5 – 10 U of Regular insulin IV bolus may be prescribed before
continuous infusion begins

Hyperglycemic Hyperosmolar Non ketotic Syndrome:

Extreme hyperglycemia without ketosis and acidosis (more than

800mg/dl)
Most often occurs in individuals with Type 1 DM
Major difference between DKA & HHNS is ketosis and acidosis do not
occur in HHNS
Assessment:
Blood glucose level ranges from 600 – 1000 mg/dl
Hypotension
Dehydration
Tachycardia
Mental status changes
Neurological deficits
Seizures
Implementation:
Fluid replacement
Correction of fluid and electrolyte imbalance
Insulin administration

93
Chronic Complications of DM

Diabetic Retinopathy:

It is a chronic progressive non inflammatory impairment of the retinal

circulation that eventually causes hemorrhage
Permanent vision changes or blindness can occur
The client has difficulty in carrying out daily task of blood glucose
testing and insulin injection
Assessment:
Change in vision due to the ruptured vessel
Sudden loss of vision as a result of retinal detachment
Blurred vision results from macular edema
Cataract results from lens opacity
Implementation:
Maintain safety
Early prevention by the control of hypertension and blood glucose level
Photocoagulation or laser therapy to remove hemorrhagic tissue to
decrease scaring

Diabetic Nephropathy

A progressive decrease in the kidney function

Assessment:
Micro albuminuria
Thirst
Fatigue
Anemia
Wt loss
Signs of mal nutrition
94
Frequent UTI
Neurogenic bladder
Implementation:
Early prevention by the control of hypertension and blood glucose level
Assess vitals
Monitor I/O
Restrict dietary protein, Na+ & K+
Prepare the client for dialysis and kidney transplantation

Diabetic Neuropathy

It is a general deterioration of nervous system.

Complications occur with foot injuries resulting from trauma and the
development of ulcers require amputation
Assessment:
Parasthesia
Decreased or absent reflex
Decreased sensation to vibration, light, touch or pain
Aching or burning in the lower extremities
Poor peripheral pulse
Skin break down and signs of infection
Loss of sensation in Cranial nerve III, IV, V & VI
Dizziness and postural hypotension
Incontinence
Impotence
Implementation:
Early prevention by the control of hypertension

95
Careful foot care to prevent trauma
Administer pain medications

96
Nervous system

97
98
Cerebro Vascular Accidents (Stroke/CVA)

It is a sudden focal neurological deficit caused by cerebro vascular

diseases.
It is a syndrome in which cerebral circulation is interrupted causing
neurological deficits.
Cerebral Anoxia lasting longer than 10mts can cause cerebral infarction
and results in irreversible damage, surrounding cerebral edema and
congestion that cause further dysfunction.
Causes
Thrombosis
Embolism
Hemorrhage from the rupture of a vessel
TIA (Transient Ischemic Attack)
Risk factors
Patients with Atherosclerosis
Hypertension
Patients on Anticoagulation therapy
DM
Stress
Obesity
Assessment
Finding depends on the area of brain affected
Lesions in the cerebral hemisphere result in manifestations on the
contra lateral side which is the side of the body opposite to the CVA

99
Symptoms:
Aphasia(Absence of speech/inability to communicate):
Expressive Aphasia: Damage occurs to the brocas area of the frontal
brain; client understands what is said but unable to communicate
Receptive Aphasia: Injury involves Wernicke’s area in the
temporoparietal area; client is unable to understand the spoken and
often the written words. Especially
Agnosia: Inability to use an object correctly
Aparaxia: Inability to carry out a purposeful activity
Hemianopsia: Blindness in half the visual field
Homonymous Hemianopsia: Blindness in the same visual field of both
eyes
Neglect Syndrome (unilateral neglect): The client is unaware of the
existence of his or her paralyzed side
Intervention
Immediate hospitalization within 3hrs of onset
Maintain patency of airway
Assess vitals; BP
Monitor for increased ICP ; high risk in 72 hrs after stroke
Position the client on the side(for the drainage of saliva) with the head
of the bed 15-30 degree elevated
Assess LOC with GCS
Maintain a quiet environment to reduce ICP
Suction as prescribed; do not suction nasally or for longer than 10
seconds to prevent increasing ICP
Insert a Foleys catheter
Administer Anticoagulants, Antiplatelets, osmotic diuretics(Manitol to

100
reduce cerebral edema), Anti hypertensives(Beta blockers – Enapril)
Establish a good form of communication
Oral hygiene

Increased ICP

An increased ICP is caused by trauma, hemorrhage, growth of tumours,

hydrocephalous, edema or inflammation
Increased ICP can impede the circulation to the brain and absorption of
CSF and affect the functioning of the nerve cells that leads to brain stem
compression and death
Assessment
Altered level of consciousness (Earliest indication)
Headache
Abnormal respiration
Slowing of pulse
Increased temperature
Vomiting
Pupillary changes
Decorticate or decerebrate posture:
Decorticate – The client flexes one or both arms on the chest and may
extend the legs stiffy indicate non functioning cortex
Decerebrate – Client stiffly extends one or both arms and possibly the
legs indicate brain stem lesion.
Positive Babinski’s reflex - Dorsiflexion of the ankle and great toe with
fanning of the other toes (indicates a disruption of the pyramidal tract)

101
Intervention
Elevate the head of the bed 30-40° as prescribed
Avoid trendlenberg position
Prevent flexion of the neck and hips
Monitor respiratory status and prevent hypoxia
Avoid Morphine Sulphate (Respiratory depressant)
Maintain body temperature to prevent shivering
Avoid environmental stimuli
Instruct the client to avoid Vulsulva manuer

Head Injury

It is a trauma to the skull results in mild to extensive damage to the

brain
Complication
Cerebral bleeding
Hematoma
Uncontrolled ICP
Infection
Seizures
Changes in the personality or behavior
Cranial nerve deficit
Recidual deficit depends on the area and extent of damage
Types: Open and closed
Concussion: jarring of the brain within the skull with temporary loss of
consciousness
Contusion: bruising type of injury to the brain that may cause subdural
or extra dural collection of blood

102
Laceration: Scalp profusely bleeds
Skull fractures: linear, depressed, compound, comminuted
Hematoma: can occur as a result of subarachnoid hemorrhage or intra
cerebral hemorrhage
Types: Epidural Hematoma and subdural hematoma

Assessment:
Increased ICP
Changes of neurological signs in the client (reflexes)
Changes in the LOC
Head ache, nausea, vomiting
Visual disturbances
Pupillary changes( dialated, unequal)
Papilledema (optic nerve damage)
Extra ocular eye movement
Nuchal rigidity (Meningitis)

Glasgow Coma Scale

1. Motor response points:

Obeys a simple response = 6
Localizes painful stimuli = 5
Normal flexion =4
Abnormal flexion(decorticate) = 3
Extensor response(decerebrate) = 2
No motor response to pain =1
2. Verbal response points:
Oriented =5

103
 Confused conversation = 4
Inappropriate words =3
Response with incomprehensible sounds = 2
No verbal response =1
3. Eye opening:
Spontaneous =4
In response to sounds =3
In response to pain =2
No response, even to painful stimuli = 1

Normal is 15
Most responsive – 10
Intermediate response – 7 to 10
Comatose – less than 7
Deep comatose – 4 to 5
Least responsive – 3
Intervention:
Clinical manifestation depends upon increased ICP
Monitor respiratory status
Maintain patent airway
Avoid administering Morphine Sulphate (respiratory depressant
and may increase ICP)
Initiate seizure precaution
Prevent neck flexion
Monitor for pain and restlessness
Monitor for drainage from the nose or ears because this fluid may
be CSF (Halosign) . Notify it to the physician

104
Spinal Cord Injury

Trauma to the spinal cord causes partial or complete disruption of

the nerve tracts or neurons
Injury can involve contusion, laceration or compression of the cord
Spinal cord edema develops and necrosis of the spinal cord occurs
as a result of compromised capillary circulation.
Loss of motor function, sensation, reflexes and bowel and bladder
control
Most common cause includes motor vehicle accidents, sporting
and industrial accidents
Complication:
Autonomic disreflexia: visceral distension of bladder
Spinal shock: absence of reflex
Further cord damages and death
Respiratory failure
The most frequently involved vertebrae are Thoracic 12, Lumbar 1,
Cervical 5 ,6&7
Assessment:
Quadriplegia: C1 – C8 Injury
Paraplegia: T1 – L4 Injury
Cervical Injuries: Injury at C2 & C3 are usually fatal (loss of
respiratory control)
C4 is the major innervations to the diaphragm by the phrenic
nerve
Involvement above C4 causes respiratory difficulty and paralysis of
all four extremities

105
Client may have movement in the shoulder if the injury is at C5 or
below
Thoracic injuries: loss of movement of the chest, bowel, trunk and
legs
Leg paralysis
Autonomic dysreflexia with lesions or injuries above T6 and
cervical lesions may occur
Lumbar and sacral level: Loss of movement and sensation of lower
extremity
S2 & S3 centre on micturition; therefore, below this level, the
bladder will contract but not empty (Neurogenic bladder)
Damages the sympathetic and parasympathetic response
preventing erection and ejaculation
Emergency management:
Emergency management is critical because improper handling can
cause further damage and loss of neurological function
Maintain patent airway
Always suspect spinal cord injury until it is ruled out
Prevent head flexion, rotation or extension
Logroll the client

Cranial Nerves
I. Olfactory: Smell; smallest Cranial Nerve
II. Optic: Vision
III. Occulomotor: Muscle movements
IV. Trochlear: Ear
V. Trigeminal: Chewing

106
 VI. Abducents: Eye movements
VII. Facial: Facial movements
VIII. Vestibulo Cochlear(Acostic): Balancing/Hearing
IX. Glosso pharyngeal: Tongue(posterior) Taste
X. Vagus: Gag reflex, Vocal cord
XI. Spinal Accessories: Reflex action/lower motor neurons
XII. Hypoglossal: Taste (Anterior tongue)

Trigeminal Neuralgia

A sensory disorder of the 5th Cranial Nerve results in severe recurrent

sharp facial pain along the Trigeminal Nerve
Assessment:
Pain on lips, gums, nose and across the cheeks
Situations that stimulate symptoms are cold, hot, washing the face,
food and fluids of extreme temperature
Implementation:
Instruct the client to avoid hot and cold fluids
Provide small feeding of fluids or soft food
Instruct the client to chew the food on the unaffected side
Administer medications like carbamazepine, phenatoin, baclofen etc.
Surgical Management:
Jannetta procedure: surgical relocation of the artery that compresses
the Trigeminal Nerve

107
Parkinson’s Disease

It is a degenerative disease caused by the depletion of dopamine which

interferes with the inhibition of excitatory movements
It is a slow progressive disease that results in crippling disability
The debilitation can result in falls, self care deficit, failure of body
system and depression
Assessment:
Bradykinesia (decreased muscle movement)
Sluggishness of physical and mental response
Aching of the shoulders and arms
Monotonous speech
Hand writing becomes progressively smaller
Tremors in hands and fingers at rest (pin rolling)
Tremors increase when fatigued and decrease with purposeful activity
or sleep
Blank facial expression
Drooling
Loss of co ordination and balance
Implementation:
Assess neurologic status
Provide high calory, high fiber diet
High protein diet interferes with the effectiveness of levodopa
Monitor for constipation
Administer Anti cholinergic medications (cogentin) to treat tremers
Administer Antiparkinsonian medications to increase the level of
dopamine(Levodopa/Carbidopa: postural hypotension-side effect)

108
Avoid food high in Vitamin B6 (interferes with anti parkinsonian
medications)

Guillain Barre Syndrome

An acute infectious neuronitis of cranial and peripheral nerves

The immune system over reacts to the infection and destroys the myelin
sheath
It is usually proceeded by a mild upper respiratory infection or a gastro
enteritis
The recovery is a slow process and can take years
Assessment:
Major concern is difficulty breathing
Parasthesia
Weakness of lower extremities
Gradual progressive weakness of the facial muscles and upper
extremities
Possible progression to respiratory failure
Cardiac Dysrhythmias
CSF reveals an elevated protein level
Abnormal EEG
Implementation:
Treatment of symptoms
Monitor respiratory status
Initiate respiratory support(SIMV)
Monitor cardiac status
Assess complications of immobility (contractures, bed sore, DVT,
Constipation, Muscular Atropy)

109
Myasthenia Gravis

It is a neuromuscular disease characterized by a considerable weakness

and abnormal fatigue of the voluntary muscle
A defect in the transmission of nerve impulses to the muscle at
myoneural junction
Causes:
Insufficient secretion of acetylcholine
Excessive secretion of cholinesterase enzyme
Unresponsiveness of muscle fibers to acetylcholine
Assessment:
Weakness and fatigue
Difficulty chewing
Disphagia
Ptosis of eyes
Diplopia
Weak and hoarse voice
Difficulty breathing
Respiratory paralysis and failure
Intervention:
Monitor respiratory status and ability to cough and deep breath
adequately
Monitor for respiratory failure
Maintain suctioning and emergency equipments at bed side
Monitor vitals, speech and swallowing ability to prevent aspiration

110
Encourage the client to sit up while eating
Instruct the client to avoid stress, infection, fatigue and over the counter
medication
Medication:
Anticholenesterase: It increases the level of acetylcholine at the
myoneural junction
Eg: Neo stigmine bromide (prostegmin), Pyudostegmin bromide
Side effects: Sweating, increased salivation, nausea, diarrhea,
abdominal cramps, bradycardia and hypotension
Intervention:
Administer medication on time
It should be administered 30mts before meals with milk or snacks to
decrease GI upset
Excessive dose leads to cholinergic crisis
Have the antidote (Atropine Sulphate) available
Cholinergic crisis results in the depolarization of the motor end plates
The crisis is caused by over medication of anticholenesterase
Assessment of Cholinergic crisis:
Abdominal cramps
Nausea, vomiting
Blurred vision
Pallor
Facial muscle twitching
Hypotension
Pupillary miosis
Intervention: prepare to administer the antidote Atropine sulphate as
prescribed

111
Myasthenic Crisis

Acute exacerbation of the disease caused by rapid unrecognized

progression of the disease caused by an inadequate amount of
medication, fatigue and stress
Assessment:
Increased pulse, respiration & BP
Anorexia
Cyanosis
Bowel and bladder incontinence
Decreased urine output
Absence of cough and swallow reflex
Intervention:
Increase the anticholenesterase medication
Tensilon test is performed to diagnose myasthenia gravis and
differentiate between cholinergic crisis and Myasthenic crisis
To diagnose Myasthenia Gravis:
Endophoneum or tensilon injection is administered. If patient shows
improvement in the muscle tone after administration, positive for
myasthenia Gravis
If patient shows no improvement in muscle strength, negative for
myasthenia Gravis
To differentiate crisis:
If the strength improves after tensilon administration, the client needs
more medication. i.e, Myasthenic crisis
Incase of cholinergic crisis, the client may be overdosed and shows no
improvement in muscle strength. Administer antidote Atropine Sulphate

112
Multiple Sclerosis

Chronic progressive and non contagious degenerative disease of the

CNS characterized by demyelinization of the neurons
It is common between the age group of 20 – 40
Cause is unknown
The disease is thought to be as a result of auto immune response or
viral infection
Assessment:
Fatigue, weakness
Ataxia
Vertigo
Tremers and spasticity of the lower extremity
Blurred vision and diplopia
Abnormal reflexes including hyper reflexia & absent reflex
Positive Babinski reflex
Memory changes and confusion
Intervention:
Provide bed rest during exacerbation
Protect the client from injury by providing safety measures
Eye patch for diplopia
promote regular elimination pattern by bowel and bladder training
Assess the need for assistive devices
Instruct the client to increase fluid intake and eat a well balanced diet
Medication: Baclofen(centrally acting skeletal muscle relaxant),
carbamazepine to treat Parasthesia

113
Corticosteroids, Methyl prednisolone to decrease edema and
inflammation
Complications:
contractures
Respiratory infection
Decubitus Ulcer

Bell’s Palsy (Facial paralysis)

Caused by lower motor neuron lesions of the VII th Cranial nerve that
may result from infection or trauma
Paralysis of one side of the face
Assessment:
Flaccid facial muscles
Inability to raise the eye brows, close the eye lids and smile
Upward movement of the eye
Loss of taste
Intervention:
Encourage facial exercise to prevent the loss of muscle tone
Protect eye from dryness( NS irrigation)
Oral care

114
Musculo skeletal system

115
116
FRACTURES

It is a break in the continuity of bone

Reduction:
Restoring bone to the proper alignment
Closed Reduction:
Performed by manual manipulation. It may be performed under LA/GA.
A cast may be applied following reduction
Open reduction:
It involves surgical intervention; may be treated with internal fixation
devices. The client may be placed in a traction or cast following the
procedure
Fixation:
Internal fixation follows open reduction. It involves the application of
screws, plate, pin or nails to hold the fragments in alignment. It may
involve removal of the damaged bone and replacement with prosthesis.
It provides immediate bone strength. Risk of infection is always
associated with procedure
External fixation: An external frame is used with multiple pins applied
through t he bones. It provides more freedom of movement than
with the traction
Traction:
Exertion of a pulling force applied in two directions to reduce and
immobilize the fracture. It provides proper bone alignment and reduce
spasm
Implementation:

117
Maintain proper body alignment
Ensure that the weight hang freely and do not touch the floor

Do not remove or lift the wt without physician’s order

Ensure that the pulleys are not obstructed and that ropes in the pulleys
move freely

Skeletal traction
Mechanically applied to the bones with pins, wires and tongs
Implementation:
Monitor colour, motion and sensation of the affected
extremity(numbness, cool & clammy skin, capillary refill)
Monitor the insertion site for redness, swelling or drainage
Provide insertion site care as prescribed
Skin traction
Traction is applied by the use of elastic bandage or adhesives
Cervical skin traction: Relieve muscle spasm and compression in the
upper extremities and neck
Use a head holder and a chin pad to attach the traction
Types:
Buck’s skin traction is used to alleviate muscle spasm and immobilize
the lower limb by maintaining a straight pull on the limb with the use of
weights. A boot is applied to attach the traction. Wt is attached to a
pulley and allow the ways to hang freely over the edge of the bed.
Not more than 8 – 10 pounds of wt should be applied
Elevate the foot of the bed to provide traction.
Pelvic skin traction is used to relieve low back ache, hip or leg pain and

118
to reduce muscle spasm. Apply traction snugly over the pelvis and iliac
crest and attached to the wt
Balance suspension traction is used with skin or skeletal traction. It is
used to approximate fracture of the femur, tibia or fibula. It is produced
by a counter force other than the client
Implementation:
Position the client in a low fowler’s or on either side of the back
Maintain a 20° angle from the thigh to the bed
Protect the skin from breakdown

CAST

It is made of plaster of paris or fiber glass to provide immobilization of

the bone and joint after a fracture
Implementation:
Keep the cast and extremity elevated
Allow a wet cast 24 – 48hrs to dry(Fiber glass cast dry in 20mts, can
move the extremity after that)
Handle a wet cast with palms of the hands until it dries. Heat can be
used to dry
Examine the skin and cast for pressure area
Monitor the extremities for circulatory impairments such as pain,
discoloration, tingling and numbness
Monitor client’s temperature
Monitor for the presence of foul odor
Monitor for the warmth on the cast(hot spot on the cast indicates
infection)

119
If an open area exists on the affected extremity, a cut out portion on the
cast or windows will be made by the physician
Instruct the client for isometric exercise to prevent muscle atropy

RHEUMATOID ARTHRITIS

It is a chronic systemic inflammatory disease due to immune complex

disorder.
The cause may be related to the combination of environment and
genetic factors lead to the distruction of the connective tissue and
synovial membranes within the joints. It weakens and leads to
dislocation of the joints and permanent deformity. Exacerbation by
physical and emotional stress
Risk factors:
Exposure to infectious agents
Fatigue and stress can exacerbate the condition
Assessment:
Inflammation
Tenderness
Stiffness of the joints
Moderate to severe pain and morning stiffness lasting longer than
30mts
Joint deformities, muscle atropy and decreased range of motion
Spongy soft feelings of the joints
Anorexia, wt loss and anemia
Low grade temperature, fatigue and weakness
120
Elevated sedimentation rate
Positive rheumatoid factor
X ray shows joint deterioration
Blood test is used to diagnose Rheumatoid arthritis (non reactive 0-39
IU/ml; reactive- more than 80IU/ml)
Medication of choice: Aspirin (Acetyl Salicylic acid); Anti coagulants
should not be taken along with Aspirin
Side effects: GI upset and prolonged BT
NSAIDs
Gold salts: It reduces remission, decrease pain and inflammation
Corticosteroids
Implementation:
Preserve joint function
Provide passive range of motion exercise to maintain joint motion and
muscle strength
Maintain balance between rest and activity
Splints during acute inflammation to prevent deformities
Prevent flexion contractures
Apply heat or cold therapy as prescribed for therapy
Apply liquid paraffin baths and massages as prescribed
Encourage consistency with the exercise programs
Instruct the client to stop exercise if pain increases
Exercise can be done only up to the point of pain
Avoid wt bearing on the inflammatory joints

OSTEO ARTHRITIS

121
Progressive degeneration of the joints as a result of wear and tear that
causes the formation of bony build up and the loss of articular cartilage
in the peripheral and axial joint. It affects the wt bearing joints and the
joints that receive the greater stress such as toes, knees and lower
spine.
The cause is unknown but may be due to trauma
Assessment:
Joint pain that intensifies after activity early in disease
As the disease progresses, pain occurs with slight motion or even at rest
Crepitus
Joint enlargement
Skeletal muscle atropy
Implementation:
Administer NSAIDs, Salycylicates, muscle relaxants
Prepare the client for corticosteroid injection in to the joints as
prescribed
Place the affected joints in a functional position
Avoid large pillows under the head or knee
Position the client in prone position twice daily
Moist heat application
Nutrition (Ca supplements)
Sugical management: Osteotomy( the bone is cut to correct the joint
deformity and promote realignment)
Total joint replacement: Hip and knee joints are commonly replaced

OSTEOPOROSIS

122
It is an age related metabolic disease
Bone demineralization results in the loss of bone mass leading to a
fragile and porous bones and subsequent fractures
Greater bone reabsorption than bone formation occurs most commonly
in wrist, hip and vertebral column
Osteoporosis can occur post menopausal as a result of metabolic
disorder or Ca deficiency
The client may be asymptomatic until the bone becomes weak that
causes fracture
Risk factors
Smoking
Early menopause
Alcohol
Family history
Female gender
Increasing age
Insufficient intake of Ca
Sedentary life style
Assessment:
The patient is possibly asymptomatic
Back pain after lifting, bending or stooping
Back pain increases with palpation
Pain in wt bearing joints such as hip and pelvis
Khyphosis ( Dowager’s hump) of the dorsal spine
Abdominal distension
Respiratory impairment as a result of movement restriction
Spinal deformity

123
Appearance of thin porous bone on X ray
Pathological fractures
Intervention:
Assess the risk of injury
Provide a safe and hazard free environment
Use side rails to prevent falls
Move the client gently when turning and repositioning
Instruct the client to use assistive devices like walkers, crutches, cane
etc.
Provide range of motion exercise
Administer estrogen and androgen to decrease bone reabsorption
Administer Ca, Vitamin D and phosphorous as prescribed for bone
metabolism
Administer calcitonin as prescribed to inhibit bone loss
Administer Analgesics, muscle relaxants & anti inflammatory as
prescribed

GOUT ARTHRITIS
It is a systemic disease in which the urate crystals deposit in joints and
other body tissues
Primary gout leads to the abnormal amount of uric acid in the body
It occurs as a result of disorder of purine metabolism
Secondary gout involves excessive uric acid in the blood that is caused
by another disease
Assessment:
Asymptomatic
S.Uric acid will be elevated
Acute phase:

124
The client has excruciating pain and inflammation in one or more small
joints especially the great toe
Chronic phase:
Chronic gout results from the repeated episodes of acute gout
Urate crystals under the skin and within the major organs especially the
renal system
Excruciating pain in the joints
Swelling and inflammation of the joints
low grade fever
Pruritis
Presence of renal stones
Increased uric acid level
Implementation:
Avoid purine containing diets(Roe, Organ meat, wine, aged cheese etc.)
High fluid intake of 2000ml/day
Wt reduction diet
Avoid alcohol and starvation diets
Increase urinary PH by eating alkaline ash diet like citrus fruits and
juices, milk and other dairy products
Monitor joint’s range of motion ability
Elevate the affected extremity
Position the joint in mild flexion during acute attack
Protect the affected joint from excessive movement or direct contact
with sheets or blankets
Heat or cold local treatment
Administer NSAIDs and anti gout medications (Allopurinol/Zyloprim,
Colchicine, Probenecid/Benemide)

125
CRUTCH WALKING

Four point gait:

Sequence:
Advance Left crutch; Advance right foot; Advance right crutch; Advance
left foot
Advantages:
Most stable crutch gait
Partial wt bearing on both legs

Three point gait:

Advance both crutches forward with the affected leg and shift weight to
the crutches. Then advance unaffected leg and shift wt on to it
Advantage:
Allow the affected leg to be partially or completely free of weight
bearing
Two point gait:
Advance left crutch and right foot; then advance right crutch and left
foot
Advantages:
Faster version of four point gait
More normal walking pattern

COMPARTMENT SYNDROME

Increased pressure within one or more compartments causing massive

compromise of circulation to an area
This results in decreased perfusion and tissue anoxia

126
Causes irreversible damage within 4 – 6 hrs if not treated
Assessment:
Increased pain and swelling
Pain with passive motion
Inability to move joints
Loss of sensation
Pulselessness (distal)
Intervention:
Notify the physician
Fasciotomy to relieve pressure and restore tissue perfusion
Loosen tight dressings or bivalve restrictive cast as prescribed

HIP FRACTURE

Intra capsular:
Femoral head is broken within the joint
Skin traction is applied preoperatively to immobilize and to reduce
fracture
Treatment includes THR or internal fixation with the replacement of
femoral head with prosthesis
Avoid hip flexion to prevent displacement
Extra capsular:
Fracture can occur at the greater trochanter or an intra trochanteric
fracture
Balance suspension traction is applied
Avoid hip flexion
Surgical treatment includes internal fixation with nail screws and wires

127
Management:
Maintain leg and hip in a proper alignment
Prevent flexion and internal or external rotation
Do not position on the affected side
Maintain leg adduction to prevent internal or external rotation
Use trochanter rolls to prevent internal or external rotation
Elevate head of the bed 35 - 45° for meals only
Ambulate as prescribed
Avoid wt bearing on affected leg
Use walkers (3 point gait)
Monitor wound for infection or hemorrhage
Monitor circulation and sensation of the affected side
Maintain hemovac or Jackson Pratt drain
Drainage should occur consistently 80 ml every 8hrs until 48hrs post op
Use anti embolism stockings
Avoid crossing or bending of the legs
Physiotherapy as prescribed

128
Eye and ear

129
EAR

130
Function: Hearing and maintenance of balance
1. Conductive hearing loss:
It occurs when sound waves are blocked to the inner ear fibres because
of external or middle ear disorders
Disorder can be corrected with no damage to hearing or
minimal/permenant hearing loss
Causes:
Inflammation
Tumours
Build up of scar tissue on the ossicles from previous middle ear surgery
2. Sensory neural hearing loss
A pathological process of inner ear or sensory fibers that lead to the
cerebral cortex and is often permanent
Management:
Cochlear implantation
Causes:
Damage to the inner ear structure
Damage to the Cranial nerve VIII (vestibulo cochlear)
Prolonged exposure to loud noise
Certain medications (Gentamycin)
Infections
Menier’s disease
DM

131
Myxedima
3. Mixed hearing loss/Conductive sensory Neuron hearing loss

4. Presbycusis
Associated with aging
It leads to degeneration or atrophy of the ganglion cells in the
cochlear and loss of elasticity of the basilar membrane. It also
leads to compromised vascular supply to the inner ear structure
Assessment:
Hearing loss is gradual and bilateral
Client states that he or she has no problem with hearing but
cannot understand what the words are

OTITIS MEDIA
A chronic infective inflammatory or allergic response involving the
structure of middle ear
Surgical treatment is necessary to restore hearing
Types of surgery can vary and include:
A simple reconstruction of the tympanic membrane
(myringoplasty) or replacement of ossicles within the middle ear
Tympanoplasty is the reconstruction of the middle ear and may be
attempted to improve conductive hearing loss
Pre operative:
Administer Antibiotic drops
Clean the ear of debris as prescribed
Irrigate the ear with the solution of equal parts of vinegar and
sterile water as prescribed to restore the normal PH of ear
Post operative:

132
Instruct the client that initial hearing after surgery is diminished
because of packing of the ear canal and hearing improvement will
occur after the ear canal packing is removed
Keep the dressing clean and dry
Position: flat with operated ear up for at least 12 hrs
Administer antibiotics

MASTOIDITIS

It may be acute or chronic and results from untreated or

inadequately treated chronic or acute otitis media
The pain is not relieved by myringotomy
Assessment:
Swelling behind the ear and pain with minimal movement of head
Cellulitis on the skin or external scalp over the mastoid process
Reddened, dull, thick & immobile tympanic membrane with or
without perforation
Tender and enlarged post auricular lymph node
Low grade fever
Malaise
Anorexia
Implementation:
Prepare the client for the surgical removal of infected material
Monitor for complication
Simple/modified radical mastoidectomy
Tympanoplasty is the most common treatment
Once infected tissue is removed, tympanoplasty is performed to

133
reconstruct the ossicles and the tympanic membrane and an
attempt to restore hearing is made
Monitor for dizziness
Monitor for s/s of meningitis such as nuchal rigidity, photophobia,
chills, fever and anorexia
Wound dressing should be changed every 24 hrs
Monitor the incision for edema, drainage and redness
Assist the client from getting out of bed to prevent falling and
injury from dizziness
Position the client flat with operated side up

OTOSCLEROSIS

Disease of the capsule of the middle ear that results in the bony
over growth of the tissue surrounding the ossicles causes the
development of irregular new bone formation and causes fixation
of bone.
The cause is not known, though it has a familial tendency
Non surgical intervention promotes the implementation of hearing
through amplification
Surgical intervention is the removal of bony growth that may
cause hearing loss
Assessment:
Slow, progressive, conductive & bilateral hearing loss
Schwartze’s sign: pinkish discolouration of the tymphanic
membrane which indicates vascular changes in the ear
Positive rinne test:

134
The vibrating stem is placed on the client’s mastoid process and
the client is asked to indicate when he or she no longer hears the
sound. The client normally continues to hear the sound two times
longer in front of the pinnae. Such results are positive rinne test.
If the client is unable to hear the sound through the ear in front of
the pinnae, the client may have conductive hearing loss. In this
situation the bone conduction is greater than air conduction, i.e.
negative rinne test
Weber’s tunic fork test:
Place the vibrating tunic fork stem in the middle of the client’s
head at the midline of the forehead or upper lip over the teeth.
The client is asked whether the sound is heard equally in both the
ears or the sound is louder in one ear. If the client hears the sound
louder in one ear, the term lateralization is applied on the side
hearing the loudest. Such finding indicates that the client has
conductive hearing loss in the ear to which the sound is lateralized
Positive Rombrg’s sign:
The client is asked to stand with his feet together and arms
hanging loosely at the side and eyes closed. The client normally
remains erect with only a slight swine
Surgical intervention:
Fenestration(stapedectomy): Removal of stapis with a small hole
drilled in to the foot plate and a prosthesis is connected between
incus and foot plate
Complications:
Complete hearing loss
Prolonged vertigo

135
Infection
Facial nerve damage
Implementation:
Instruct the client in measures to prevent middle ear or external
ear infection
Instruct the client to avoid excessive nose blowing
Not to clean the ear canal with buds or sharp objects
Post op:
Inform the client that hearing is initially worse after the surgical
procedure because of swelling that no noticeable improvement in
hearing may occur for as long as 6 weeks
Assist with ambulation during first two days after surgery
Instruct the client to move the head slowly when changing
position to prevent vertigo
Instruct the client to avoid people with Upper Respiratory Infection
Instruct the client to avoid middle ear pressure because it can
dislodge the graft or prosthesis

MENIER’S DISEASE
It is also called as Endolymphatic hydrox and refers to the
dialation of endolymphatic system by over production or
decreased reabsorption of endo lymphatic fluid.
Assessment:
Tinnitus (mask it with low level competing music in case of chronic
tinnitus)
Vertigo, nausea and vomiting
Feeling of fullness

136
 Unilateral sensory neural hearing loss
Symptoms occur in attacks and last for several days
Initially, hearing loss is reversible but as the frequency of attack
continues hearing loss will be permenant
Repeated damage to the cochlear caused by increased fluid
pressure leads to permenant hearing loss
Nistagmus (Oscillating movement of the eye)
Head ache
Causes:
Any factor that increases endolymphatic secretion
Viral and bacterial infections
Allergic reactions
Vascular disturbances producing changes in the micro circulation
in the labyrinth
Biochemical disturbances
Implementation:
Prevent injury during vertigo attacks and provide bed rest with
quiet environment
Provide assistance with walking
Initiate Na+ and water restriction
Instruct the client to stop smoking
Tranquilizers and sedatives to calm down the patient
Surgical management:
Endolymphatic drainage and insertion of a shunt which may be
performed early in the course of disease to assist with the
drainage of excess fluid

ACOSTIC NEUROMA

137
A benign tumor of the vestibule or acostic nerve which may
damage hearing and affects the facial movement
Treatment includes surgical removal of the tumor through
craniotomy. Tumor rarely reoccurs after surgery

FOREIGN BODIES IN THE EAR

Foreign bodies include vegetable, beeds, pencil lid, insects etc.

Assessment:
Sensation of fullness in ear with or without hearing loss
Pain, itching and bleeding
Implementation:
If the foreign object is vegetable, irrigation is done with care
because material expands with hydration
Insects are killed before removing. Mineral oil or alcohol is instilled
to suffocate the insect which then removed by forceps

138
EYE

139
CATARACT

Cataract is an opacity of the lens that distorts the image projected in to

the retina and that can progress to blindness
Causes:
Aging process (senile cataract)
Inheritted (Congenital cataract)
Injury ((Traumatic cataract)
It can also result from another eye diseases (Secondary cataract)
It is asymptomatic and intervention is indicated when visual
aquity has been reduced to a level that the client finds to be
unacceptable and adversely affect the lifestyle
Assessment:
Opaque or cloudy white pupil
Gradual loss of vision
Decreased colour perception
Vision that is better in dimlight with pupil dialation
Photophobia
Absence of red reflex
Intervention:
Surgical removal of the lens : One eye at a time is performed
ICCE (Intra Capsular Cataract Extraction)
ECCE ( Extra Capsular Cataract Extraction)
In ECCE, the lens is lifted out without removing the lens capsule. The
procedure may be performed by phaco emulsification in which the lens
is broken up by ultra sonic vibration and is extracted

140
In ICCE, the lens is removed with it’s capsule through a small incision. A
partial iredectomy may be performed with the lens extraction to
prevent acute secondary glaucoma.
A lens implantation may be performed at the time of surgery procedure
Instruct the client regarding the post op measures to prevent or
decrease IOP (Don’t bend, can lift less than 5-10 pounds wt)
Administering eye medication pre operatively including Mydreatics
(Pupillary dialation/ for increased IOP) and Cycloplegics

Post op:
Elevate the head end 30 -400
Turn the client to the back or unoperated side
Maintain eye patch; both eyes to limit movements
Orient the client to the environment
Position the client’s personal belongings to the unoperative side
Use side rails for safety

GLUCOMA

Increased IOP (Normal 10 – 21 mmHg) due to the inadequate drainage

of acqueous humour from the canal of schelemen or the over
production of acqueous humour
Condition damages the optic nerve and results in blindness
Types:
Acute closed angle or narrow angle glaucoma: results from the
obstruction to the outflow of the acqueous humour
Chronic closed angle glaucoma: follows an untreated attack of acute
closed angle glaucoma

141
Chronic open angle glaucoma: results from over production or
obstruction to the outflow of acqueous humour
Increased IOP as a result of increased resistance of acqueous humour
out flow through the trabicular meshwork canal of schelemen and
episcleral venous system
Acute glaucoma has rapid onset; IOP is above 50 - 70 mmHg
Chronic glaucoma is slow progressive; IOP is more than 30 -50mmHg
Assessment:
Progressive loss of peripheral vision followed by loss of central vision
Increased IOP
Vision worsening in the evening with difficulty adjusting to dark room
Blurred vision
Hallows around the light
Lacrimation
Progressive loss of central vision
Implementation:
Acute should be treated as a medical emergency
Administer medication as prescribed to decrease IOP
Prepare the client for peripheral iridectomy. It allows acqueous humour
to flow from posterior to anterior chamber.
For chronic, instruct the client about the importance of medication
Miotics to constrict pupil
Carbonic unhydrates inhibit the production of acquous humour
Beta blockers inhibit the production of acquous humour
Instruct the client to take life long medication
Avoid anti cholinergic medication

142
Traviculoplasty allows the drainage of acquous humour in to
conjunctiva.

RETINAL DETACHMENT

Occurs when the layer of the retina separates because of the

accumulation of fluid between them or elevation of both retinal layers
away from the choroid as a result of tumour
Partial separation becomes complete if untreated
Complete detachment results in blindness
Assessment
Flashes of light
Floaters
Blurred vision
Sense of curtain being drawn
Loss of portion of visual fields
Implementation
Provide bed rest
Cover both eyes to prevent further detachment
Speak to the client before approach
Avoid jerky head movement to minimize eye stress
Protect the client from injuries
Drainage fluid from the sub retinal space. So that the retina can return
to its normal position
Crio surgery
Diathermy
Laser therapy

143
Scleral buckling to hold the choroid and retina together with a splint
until the scar tissue formed closing the tear
Post op management:
Apply eye patches bilaterally
Monitor for hemorrhage
Monitor for sudden sharp pain
Administer eye medication
Avoid sudden movement of the head
Instruct the client to avoid straining, lifting and bending on the waist
Instruct the client to wear dark glasses day time and eye patches at
night

FOREIGN BODIES

Objects such as dust or dirt that enters the eye

Implementation:
Have the client to look upward; expose the lower lid; wet a cotton
tipped applicator with sterile NS and gently twist the swab over the
particle and remove it
If the particle cannot be seen, have the client look downward; place a
cotton applicator horizontally on the outer surface of the upper eyelid,
grasp the lashes and pull the upper lid outward and over the cotton
applicator; if the particle is seen, gently twist the swab over it to remove
Penetrating objects
Injury that occurs to the eye in which an object penetrates the eye
Implementation:
Never remove the object because it may be holding ocular structures in
place; the object must be removed by the physician

144
Cover the object with a cup
Do not allow the client to bend
Do not place pressure on eye

Chemical burns

An eye injury in which a causative substance enters the eye

Implementation:
Treatment should begin immediately
Flush the eye of injury with water for at least 15-20mts
At the scene of injury, obtain a sample of the chemical involved
At the ER, the eye is irrigated with NS or an ophthalmic irrigation
solution
The solution is directed across the cornea and towards the lateral
canthus
Apply antibiotic cream as prescribed

Exentration and Enucleation

Enucleation: removal of the entire eyeball

Exentration: removal of the eyeball and surrou
nding tissues and bones
Perfom for the removal of ocular tumour
After the eye removal, ball implant is inserted to facilitate best cosmetic
results

145
146