Medical Sursical III NotesVIP

Medical surgical Nursing-III
UNIT NO: 1: NEUROLOGICAL NURSING

Assessment of neurological System
A) Examination of mental status: -

Presence of organic brain diseases can be observed by level of consciousness ( L.O.C), which is most
sensitive indicator of brain abnormality. The function components are 1. Arousal (alertness) 2.
Awareness (consent) of self & environment. Arousal is controlled by brain stem activity & awareness
by cerebral cortex.
Arousal is determined by eye opening – A painful stimuli can be applied to the eye, whether the
arousal of intact or not.
Awareness is determined by patient orientation to person, place & time.
B) Language & Speech:-

Language ability is controlled on the cortical field includes parts of temporal lobe, temporo-
perietlooccipital junction, frontal lobe. Impairment in language ability may be aphasia or dysarthria.
1. Aphasia: deficiency or loss of ability to express one self or understand Language.
 Motor expression includes impairment of ability to speak and write patient can understand
spoken & written words.
 In anomic aphasia patient is unable to name the objects.
 Sensory (Receptive) aphasia refers to impairment to understand the spoken words due to
disease of auditory & visual center damage.
 Mixed Aphasia:- Combined expressive & receptive aphasias
2. Dysarthria: - This is indistinctness in word articulation result due to interference with
peripheral speech mechanism ( the tongue, palate, pharynx, lips etc).
C. Perception :
Sensation is integrated in the sensory cortex especially in parietal lobe. The ability to recognize the
object is impaired. Recognition is observed by any sense e.g. sterognosis, the ability to perceive the
object by touch. Absence of ability is called “agnosia”.
Aprexia is another perceptual problem refers to inability to perform skillful, purposeful motor
function.
-Constructional Aprexia :- impairment in producing designs in two or three dimension to copying,
drawing or constructing may be due to damage of occipitoparietal lobe.
-Dressing Aprexia :- patient can not dress accurately due to lesion in occipital or parietal lobe.
-Idomotor Aprexia :- unable to imitate gestures or perform a purposeful motor task on command. It is
due to lesion in parietal lobe.
-Kinesthetic Aprexia:- It is loss of kinesthetic memory pattern. Patient is unable to perform a
purposeful motor task although it is understood.
D. Sensory status:-
This depends on patient co-operation, alertness and responsiveness. The person should be relaxed with
eyes closed to avoid recovering visual clues sensation should be tested to both sides of same area.
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Nursing Instructor SON Male Jacobabad
E. Assessment of Cranial Nerves: -
a) Olfactory nerve: - (Cr-1)
test for smell- ask the patient to close one nostril and close the eyes and sniff from bottle.
b) Optic nerve: - ( Cr-2)
Observe by visual field and visual acuity
c) Occulumotor, trochlear & abducens :- (Cr-3,4,6)
check the eye movement & movement of extraoccular muscle.
d) Trigeminal nerve :- (Cr-5)
The sensory part can be examined by touching or pricking, ophthalmic, maxillary & mandibular areas.
e) Facial nerve :- (Cr-7) mixed
ask the patient to smile, close both eyes, look upward, wrinkle the forehead, show the teeth. In
abnormality patient will unable to do these activities.
f) Acoustic nerve :- (Cr-8)
it is tested by turning fork
g) Glosso Pharygeal & Vagus nerve:-
supplies to posterior to pharyngeal wall, normally when wall is touched there is a contraction of the
muscles.
h) Hypoglossal nerve :-
motor nerve, tongue is firstly inspected if any lesion is present tongue deviated to that lesion.
F. Motor Status: -
Gait & stance are complex activities require muscle strength, coordination and balance. Ataxia refers
to the lack of coordination and purposeful walking. For assessment patient is asked to walk naturally
then on heal to toe in straight line.
To evaluate stance patient is asked to close the eyes and then close the feet together. If patient has no
problem, he can stand with balance.
For muscle strength ask the patient to grasp the nurses both hands and then squeeze them
simultaneously.
For testing the co-ordination ask the patient to touch the nose then touch the doctor / nurses hand.
Normally he can do that.
A. Reflexes :-
This is predictable response that resulting from nerve input over reflex are tendon.
Four points are important for that
0 = absent
1 = Weak response
2 = Normal response
3 = Exaggerated response
4 = Hyper reflexia with colonies
we observe reflex in calcaneal tendon of soleous muscle, Bicep reflex in bicep tendon, triceps in
triceps tendon, patellar in patella tendon, kerning reflex and brudzinski reflex
The Common diagnostic studies are:

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1. Cerebro spinal fluid analysis :-

C.S.F is a clear fluid that is formed in the third fourth and lateral ventricle of brain. Sample is obtained
by lumber puncture to examine its constituents and foreign substance. Such as pathogenic organism,
blood etc.
Normal C.S.F values are:
Specific gravity 1.007
Ph 7.35
Appearances clear, colorless
RBCs None
WBCs 0.008/L
Pressure 75-180 mm of H2O
Protein lumber 15-45 mg/dl
Cisternal 15-25 mg/dl
Ventricular 5-15 mg/dl
Glucose 45-75 mg/dl
Micro-organism Non
Diagnostic Tests
2. C.T Scan : -
This makes use of narrow beam of x-ray to scan head in successive layers. The images that are
produced provide cross sectional view of the brain with distinguish difference in tissue densities of the
skull, cortex, sub-cortical structure & ventricles. The image is displayed on a T.V monitor & is
photographed. Lesions in brain are seen variations in tissue density differing from normal brain tissue.
Possible tumor masses, brain infarction, displacement of the ventricle etc can be observed. The patient
lies fixed on the adjustable table while scanning system rotates around the head. It is non-invasive,
painless & high degree of sensitivity for detecting lesion
Patient preparation involves explaining the test producer and teaching about procedure. Patient is also
taught about some sensation like light heatedness, dizziness etc. relaxing techniques should be
introduced to relieve anxiety. Removing jewelry or other material from neck, ears etc.
3. Magnetic Resonance Image (MRI): -

MRI uses a powerful magnetic field to obtain images of different areas of body. MRI has the potential
for identifying cerebral abnormality earlier & clearer than other tests. It can provide information about
chemical changes within cells. It doesn’t require ionization radiation.
 Patient’s all the metallic object e.g. jewelry, rings, watches, hair pin must be removed as
well as credit cards.
 A complete history is also obtained for any metallic hardware in bones, muscles etc should
be taken.
 These objects may malfunction or heat up as they absorb radiation.
 Patient should be educated for thumping of magnetic coil as the magnetic field is being
pulsed.
 Teach the patient about the relaxing techniques.
 This procedure is painless. The patient lies on the flat platform that is moved into a tube
containing the magnet.
4. Cerebral Angiography: -
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Cerebral angiography is an x-ray study of cerebral circulation after contrast medium has been injected
into selected artery. This is a valuable tool for investigating vascular disease and arteriovenous
malformation.
Patient Preparation: -
 Patient should be well hydrate, and clear liquids are usually permitted up to the time of
study.
 Instruct the patient to remain immobile during the imaging procedure.
 Be sure that groin area is shaved for procedure.
 Observe the injection site for the hemorrhage & hematoma.
 Ice cap may be applied on the puncture site for relief.
5. Myelography: -
It is x-ray of spinal subarachnoid space following the injection of contrast agent into spinal
subarachnoid space through lumber puncture. It out lines the spinal subarachnoid spaces spinal cord,
tumor, cysts etc.
After injecting contrast medium the head is tilt down.
After Procedure:
 Patient head should be elevated 30-50 degree to reduce the rate of upward dispersion of
the medium.
 If agent used, as contrast medium is oil based patient should lie prone for 2-3 hours and
recumbent position for 12-24 hours to reduce C.S.F leakage and decrease headache.
 Check pulse, BP etc.
 Check punctured area.
 Check for any leakage.
6. Electroencephalography ( EEG) :-
It represents a record of the electrical activity generated in the brain & obtain through the electrodes
applied on scalp surface.
It is useful for testing seizure disorder such as epilepsy. It is also an indicator of brain death.
1. Before EEG tranquilizers should be with held 24-48 hours before procedure.
2. Coffee, tea, cola, drinks should be omitted in the meal before test.
3. Inform the patient procedure will take 45-60 minutes.
4. Inform patient that it does not cause electric shock
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1) Parkinsonism or Parkinson’s disease
It is neuromuscular disorder caused by deficiency of Dopamine level in body due to decreased
production of dopamine by dopaminergic neurons
Parkinsonism is the name given to a disturbance of motor function characterized by expressionless
faces, a stooped posture, slowness of voluntary movement festinating gait (progressively shorter
accelerated steps), muscle rigidity and pill rolling tremors. This disease was named Parkinsonism
because of after the work of James Parkinson, who wrote on “shaking palsy” in 1817. which now
called as idiopathic Parkinsonism
Causes: -
 This disease affects the men & women usually after the age of 50 years.
 Genetic factor
 Antipsychotic medication.
 Encephalitis
 Ischemia
 Neurotoxins such carbon monoxide
Pathogenesis:-
The dopaminergic neurons of the substantia Nigra project to striatum and their degeneration on
Parkinson’s disease is associated with the reduction in the striatal dopamine content with in the basal
ganglia. Dopamine is neurotransmitter responsible for controlling the motor movement. Dopamine has
inhibitory effect & acetylcholine has an exciting effect. When the exciting activity of acetylcholine is
inadequate balance by dopamine & individual has difficulty in controlling and initiating voluntary
movement Parkinsonism disease causes extra pyramidal tract impairment that control the movement.
Clinical Findings:-
 Tremors
 Rigidity
 Bradykinesia (slow movement)
 Expressionless faces
 Stooped posture
 Shortened accelerated steps
 Pill rolling tremors
 Widened palpebral fissure
 Repetitive tapping: over bridge of nose
 Semi flexed arms
 Produce sustained blink response
 Difficulty in initiating movement.
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Complications:-
 Dysphagia
 Orthostatic hypotension.
 Constipation.
 Insomnia
 Akinesia
 Blurred vision.
 Depression.
 Loss of memory.
 Dementia.
 Fainting syncope.
Rx:-
 Levodopa + Carbidopa ( sinement) firstly 100/25 mg Tab. T.D.S then
Dosage can be increased.
 Kemardin (Anticholenergic) mostly drug induce 2.5mg T.D.S.
 Dopamine agonist (Bromocriptine) parlodel 2.5mg. 1-1.25mg at bed time Week , 2-
2.5mg at bed time Week 2, 2.5mg B.D Week 3, 2.5mg T.D.S Week 4
Side effects of Dopamine Drugs:-
 Orthostatic hypotension.
 Nausea & vomiting.
 Hallucination.
 Toxic psychosis
 Agitation
 Dizziness
 Palpitation
 Delusion
 Dry mouth
 Confusion
 Sleep disturbance
Nursing Care:-
1. Perform range of motion exercise to all joints for three times daily.
2. Massage & stretch muscles to reduce stiffness.
3. Pay attention to posture. Try to walk with the hands clasped behind.
4. Avoid staying on one position for prolonged time and keep altering position regularly.
5. Reduce the risk of injury by advising use of assistive device.
6. Monitor weight once a week.
7. Evaluate Dysphagia and modify diet to increase case chewing and swallowing.
8. Avoid high protein meal at time of medication.
9. Ensure adequate fiber diet and fluid intake to prevent constipation.
10. Use stool softeners if needed.
11. Monitor for depression.
12. Educate the patient about therapy & its side effects.
13. Avoid vitamin supplement with products that contain vitamin B6 (pyridoxine) because it
increase the conversion of Levodopa in liver, which decrease the amount of available for
conversion to dopamine in brain.
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2) Myasthenia Gravis
Myasthenia gravis is neuromuscular disorder thought to be due to the presence of an antibody against
acetylcholine receptors at the neuromuscular junction, characterized by abnormal fatigability.
Classification
Class I: Any eye muscle weakness, possible ptosis, no other evidence of muscle weakness elsewhere
Class II: Eye muscle weakness of any severity, mild weakness of other muscles
Class III: Eye muscle weakness of any severity Moderate weakness of other muscles
Class IV: Eye muscle weakness of any severity, severe weakness of other muscles
Class V: Intubations needed to maintain airway
Causes:-
 Auto antibodies (HLADr3).
 Thyrotoxicosis.
 Thymoma (tumor of the thymus gland).
 Rheumatic Arthritis
 Family History.
Pathophysiology
Myasthenia gravis is an autoimmune disease. There is a slight genetic predisposition: particular HLA
types seem to predispose for MG (B8 and DR3 with DR1 more specific for ocular myasthenia). Up to
75% of patients have an abnormality of the thymus; 25% have a thymoma, a tumor (either benign or
malignant) of the thymus, and other abnormalities are frequently found.In MG, the auto antibodies are
directed most commonly against the acetylcholine receptor (nicotinic type), the receptor in the motor
end plate for the neurotransmitter acetylcholine that stimulates muscular contraction. Some forms of
the antibody impair the ability of acetylcholine to bind to receptors
Sign & symptoms:-

 Fluctuating, weakness of commonly used voluntary muscles.
 Extreme muscular weakness & easy fatigability.
 Generally symptoms are worse after efforts/ activity and relieved by rest.
 Slightly exertion as combing the hair, chewing, talking stop due to weakness.
 Involvement of ocular muscles causes diplopia and ptosis.
 Difficulty in breathing
 Limb weakness.
 Dysphagia (difficulty in swallowing),
 shortness of breath
 Dysarthria (impaired speech)
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Diagnostic Evaluation:-
 Chest x-rays to demonstrate coexisting thymoma.
 Injection of edrophonium ( Tensilon), facilitates transmission of impulses to myoneural
junction with in 30 seconds of injection, myasthenia gravis patients improve the severity of
disease.
 Serum HLA antigen Dr3.
Medication :-
 Anticholenestrase drugs provides symptomatic relief, with out influencing the course of
disease - Pyridostigmine 30-180mg (averge 60mg) 4 times daily.
 Thymectomy usually leads to asymptomatic relief should be considered in all patients.
 Cortisone is indicated in patients who poorly response to pyridostgmine.
Nursing Care :-
 When there is severe weakness of abdominal and chest muscles, patients feels difficulty in
coughing and breathing. Chest physical therapy including postural drainage to mobilize the
secretion and suction to remove the secretions.
 Patient should take medicine 30 minutes before meal for maximal muscle strength.
 Plan adequate rest throughout day.
 Setting a daily schedule and spacing the activities.
 Extreme muscular activities should be avoided.
 Artificial tears in the eyes are administrated to prevent from corneal injury when eyelids do
not close completely.
 Patient is assessed for drooling, regurgitation, chocking, suctioning should be ready because
aspiration of material may occur.
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Trigeminal Neuralgia (Tic Douloureux)
Trigeminal neuralgia affects the fifth cranial nerve causes intense paroxymal pain in one or
more branches trigeminal nerves. CNS has both motor and sensory branches. The sensory
branches are involve in trigeminal neuralgia. Primarily, the maxillary and mandibular
branches. The pain is similar to electric shock or a burning sensation.
Causes:-
No etiology has been found for the disorder although risk factors have been identified. Major
initiating pathologic events may include :
 Nerve compression
 Herpes virus infection
 Infection of teeth and jaw
Clinical Findings :-
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1. contraction of some facial muscles such as sudden close of eyes twist of mouth.Hence
named as tic douloureux (painful twist)
2. The pain of this neuralgia is felt in the skin, not in deep structures.
3. The attacks are said to feel like stabbing electric shocks, burning, pressing, crushing or
shooting pain that
4. Various triggers may commonly precipitate a pain attack.
5. Light touch or vibration is the most provocative.
6. Activities such as shaving, face washing, or chewing often trigger an episode
7. A draft of cold air and direct pressure against the nerve trunk may also cause pain.
Slightly touch may start a paroxysm.
Management :-
The anticonvulsant agent such as Carba mazepine (Tegretal) and Phenytoin (Dilantin) relieve the pain
in most patient by reducing the transmission of impulses at certain nerve terminals. If pain does not
relieve the surgery is done i.e. percutaneous radio frequency rhizotomy for total pain relief. Gama
Knife radio surgery, Retrogasserion rhizotomy for permanent anesthesia Micro vascular
decompressing for pain relieving with out loss of sensation.
Nursing care of patient with trigeminal neuralgia include recognizing that certain factors may
aggravate the pain such as food that is too hot or too cold. The nurse can prevent or reduce this pain in
variety of ways such as providing cotton pads and room temperature water for washing the patient’s
face. Instruct the patient to take food and water at room temperature, to chew on unaffected side.
Introduction of Trigeminal Nerve :-
Trigeminal nerves has both functions
 Sensory &Motor
Sensory :-The sensory part of this nerve has three branches:
1. Ophthalmic
2. Maxillary
3. Mandibular
1. Ophthalmic :-This branch is supplied to the following parts :
 Orbit of the eye
 Eyelid
 Eye brow
 Skin of forehead
 Nose
2. Maxillary :-This branch is supplied to the following parts :
 Upper teeth
 Lower eyelid
 Cheek
 Upper palate
 Upper lip
 Upper gums
3. Mandibular: -This branch is supplied to the following parts :
 Lower gums
 Salivary glands
 Lower teeth and lower lips
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Bell’s Palsy (Facial Paralysis)
This refers to a peripheral facial paralysis characterized by a disruption of motor branch of

facial nerve (CN VII) or one side of face in the absence of other disease such as stroke. The
disorder causes weakness or paralysis of facial muscles.
Causes: -The appropriate cause is unknown. But some causes are
Trauma: Physical trauma,
Tumour: facial neuromas, congenital cholesteatomas, acoustic neuromas, parotid gland neoplasms,
Herpes zoster:Herpes zoster is essentially a herpes zoster infection that affects cranial nerves VII
(facial nerve) and VIII (vestibulocochlear nerve).
Acute and chronic otitis media
Path physiology
A popular theory proposes that inflammation and swelling of the facial nerve results in
compression of the nerve within the temporal bone. The facial nerve courses through a portion of
the temporal bone commonly referred to as the facial canal. The first portion of the facial canal, the
labyrinthine segment,The edematous inflamed nerve becomes compression to the damage or its
nutrient vessel is occluded to the point of producing Ischemia, necrosis of nerve with in the long canal.
There is distortion of face from paralysis of facial muscles, increased lacrimation (tearing) and painful
sensation of the face, behind the ear and in the eyes. The patient is unable to speak and eat on effected
side because of weakness of the muscles.
Signs and Symptoms: -
 The onset of Bell’s palsy is often accompanied by an outbreak of herpes vesicles (Herpes:
any inflammatory skin disease marked by the formation of small vesicle in cluster to such
disease caused by herpes virus) or around the ear.
 Patient complains pain around the ear or behind the ear.
 Flaccidity of the effected side of the face.
 Drooping of the mouth.
 Unable to close the eyelids with upward movement.
 Widened palpebral fissure.
 Unable to smile.
 Unable to show the teeth.
 Unable to make the wrinkles on the forehead.
 Can’t move eyebrows upward.
 Tearing
Complications: -
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 Malnutrition.
 Dehydration.
 Corneal abrasion.
 Muscle stretching etc
.
Medical Managemet: -
 Tab. Predisone 80mg daily in divided dose for 5-7 days. Such as prednisone, are used to reduce
swelling and inflammation of the facial nerve. Whether or not this treatment speeds up healing and
improves the chances for complete recovery has not been determined. Once the decision has been
made to use corticosteroids, they should be started within 2 days after symptoms develop.
Treatment is continued for 1 to 2 weeks.
 Tab. Acyclovir (Zovirex) 200mg four times a day for 5 days. Treatment with antiviral agents such
as acyclovir may be beneficial. Acyclovir and prednisone used together are more effective than
prednisone alone. The acyclovir-prednisone combination is most effective when begun as soon as
possible after the onset of symptoms. One recent study found that patients had a 100% recovery
rate when treated within 3 days of symptom onset, compared to an 84% recovery rate when
treatment was delayed 4 days or longer
 Tab/Inj. Neurobian (B1, B6,B12) Three times daily. OR
 Tab/Inj. Methyl Cobal (B12) 1 amp. I/M three times a week.
 Tab. Paracetamol / Brufeen to relieve the pain.
Nursing Management: -
 Hot wet packs can reduce the discomfort of the herpic lesion and relieve the pain.
 Protection of the face from cold & drafts.
 Maintainace of good nutrition.
 Teach patient to chew the food on unaffected side.
 Maintainance of oral hygiene.
 Teach patient to safety use of heat & massage.
 Instruct the use of medicine.
 Teach importance protecting the eyes from infection.
 Monitor the patient for progress.
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Head Injury
Trauma to scalp, skull and brain is called head injury or Injury of the skull is called head injury.
1. Scalp Injury: -
Because of many blood vessels, the scalp bleeds profusely when injured. Trauma may result in an
abrasion, contusion, laceration etc. the areas are mostly irrigated to prevent from the infection.
2. Fracture Of Skull: -
This is break in the continuity of the skull caused by trauma. It may occur with or without damage of
brain. It is of two types. 1. Open fracture in which the dura is torn and 2. Closed fracture in which dura
is not torn.
Clinical Features: -
 Localized and persistent pain.
 Swelling in the region of fracture.
 In case of fracture of cranial base, there is hemorrhage from nose, ear.
 Some times CFS may escape out of the ear and due to involvement of durametter.
 Halo sign this indicates involvement of durametter. In this sign blood is surrounded by
CFS from ear and nose.
Diagnostic Evaluation: -
1. Skull X-ray.
2. C.T scan
3. MRI
3. Brain Injuries: -
The most important consideration in any head injury whether or not the brain has been injured. The
serious brain damage causes brain cell death due to cut of oxygen supply to tissue. Brain injury causes
intracranial hemorrhage and hematoma. C.T scanning and MRI are used evaluate the natural pare of
brain involvement.
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Clinical Features Of Head Injury: -
 Disturbance in the level of consciousness.
 Confusion
 Pain in the involved area.
 Swelling in the area of injury
 Halo sign
 Visual and sensory impairment may occur.
 Headache
 Movement disorders
 Seizures etc…
Complications: -
1. Increased intracranial pressure
2. Cerebral Edema
3. Hearing impairment
4. Hypoxia
5. Visual impairment
6. Cerebral hematoma
7. Brain ischeamia
8. Paralysis
Management: -
 Maintain the airway.
 Shave around the effected area.
 Wash and irrigate the injured part if the fracture is closed to prevent from infection.
 Administrate the Oxygen.
 Establish the I\V line.
 Administrate the I\V solution.
 Assess for shock and level of consciousness.
 Control external bleeding with sterile pressure dressing.
 Administrate the antibiotic and analgesic according to doctor’s order.
 Provide quite environment.
 Elevate the bed at 30 degree in case of increased intracranial pressure.
 Maintain electrolyte balance.
 Keep the record of intake and output.
 Provide emotional support.
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Epilepsy
Epilepsy is a common chronic neurological disorder characterized by recurrent unprovoked seizures.
Epilepsy is usually controlled, but not cured, with medication, Epilepsy is a condition, in which a
person has spontaneously recurring seizures caused by chronic defect of the brain. It may be associated
with loss of consciousness. The basic problem is thought to be an electrical disturbance in the nerve
cell in one section of brain, causing them to emit abnormal, recurring, uncontrolled discharges.
Causes: -
 Family history.
 Degenerative disease ( Alzheimer’s disease).
 Metabolic disorders.
 With drawal from drug.
 Hypoglycemia
 Hyperglycemia
 Congenital defect.
 C.N.S tumor.
Pathophysiology: -
A seizure can be cause by any process that disrupts the cell membrane stability of a neuron. The point
at which the cell membrane, becomes destabilized and uncontrollable electrical discharge begins is
called seizure threshold. In epilepsy abnormal neurons seem to undergo spontaneous firing. Any
stimulus that cause C.N.S neuron to depolarize induces tendency to spontaneous firing.
Classification: -
A. Partial Seizures: -
In this type only restricted part of one cerebral hemisphere has been activated. The ictal features
depends on the area of brain that is involved. It is divided into two types.
1. Simple partial
2. Complex partial.
a) Simple Partial: -
In this the consciousness is preserved and manifested by motor symptoms (convulsive jerking) or
sensory symptoms (paresthesis or tingling).
b)Complex: -
In this consciousness is impaired and accompanied with psychic symptoms and signs such as illusion
and hallucination.
B. Generalized Seizure: -It is of two types:
1. Absence seizure ( Petit Mal)
2. Tonic Clonic seizure ( Grand Mal)
a. Petit Mal: -
These are characterized by impairment of consciousness, with mild clonic tonic or atonic components
onset and termination attacks are abrupt. The impairment of the external awareness is so brief that
patient is unaware of it.
b. Grand Mal: -
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In this type, the seizures are characterized by sudden loss of consciousness. The patient become rigid
and falls on the ground and respiration is arrested. The tonic usually last less than one minute followed
by Clonic phase in which jerking movement occurs in the body. And then followed by coma. During
this phase tongue can be bitten.
Sign & symptoms: -

 Seizures.
 Muscle rigidity.
 Foaming from mouth.
 Tonic symptoms.
 Clonic / jerking of body.
 Unconsciousness.
 Confusion.
 Illusion.
 Hallucination.
 E.E.G.
 C.T scan.
 MRI.
Rx: -
 Phenytoin sodium 100mg B.D.
 Carbamazapine 100-200mg OD or BD.
 Or Sodium Valproate – initially 600mg daily in two divided doses usually maintain 1-2
daily.
Nursing Care: -
 Ensure patient’s airway.
 Suction as needed.
 Stay with patient until seizures has passed.
 Place mouth gag or pencil or other substance between teeth to prevent from tongue
bitten.
 Remove all the sharp things from place.
 Keep the patient on ground.
 Remove or loose tight clothes.
 Monitor vital L.O.C.
 Educate the patient for following:
a) Medication must be taken as prescribed.
b) Avoid from driving.
c) Avoid from swimming in canal / tube well.
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Increased Intra cranial Pressure
Normal intra cranial is the pressure that is exerted by the total volume from three components with in
the skull, these are brain tissue, intra cranial blood volume and cerebrospinal fluid. Normal intra
cranial pressure in lateral position is 60-150 mm of H2O & in 30 degree head elated is 0-50 mm of
H2O. The rigid cranial vault contains 1400 grams of brain tissue, 75 ml blood and 70 ml C.S.F
Under normal condition minor changes may occur due to coughing, sneezing, straining etc.
Pathological condition causes I.I.C.P: -
a) Head injury
b) Brain tumor
c) Cerebral edema.
d) Brain hemorrhage.
e) Brain Ischaemia.
f) Stroke
g) Intra cranial surgery.
h) Brain infection.
Pathophysiology: -
According to Monro-Killie hypothesis, any condition that increase one or more of intra cranial
content must cause reciprocal change in the remaining contents. And increase intra cranial
pressure occurs. As intra cranial volume increase, the compensatory mechanism takes place.
C.S.F filled space are compressed by surrounding brain tissue and distribute the C.S.F to
lumber and also blood vessels especially veins. These compensatory mechanisms maintain the
equilibrium. But these mechanisms are exhausted when changes are continuous, when volume
overwhelms, the compensatory system, the intra cranial pressure rises.
As pressure with in skull increase, the cerebral blood vessels are compressed, causing
reduction in cerebral blood flow and result in Ischaemia. If this Ischaemia occurs 3-5 minutes,
the brain is suffer irreversible damage.
Brain Death: -
Cessation of blood flow results in cerebral hypoxia leading to brain death.
 Altered level of consciousness.
 Spontaneous movement, movement caused by noxious stimuli such as pinching and
injection.
 Severe headache, which is constant.
 Purposeless movement.
 Increased blood pressure.
 Increased temperature / fever.
 Decreased pulse.
 Decreased breathing.
 Arterial hypertension.
 Widens pulse pressure.
 Recurrent projectile vomiting.
 Decorticate posture; involve adduction and flexion upper extremities and planter flexion of
the feet.
 Decerbrate position: - extension and outward rotation of upper extremities and plantar
flexion of the feet.
Sakhawat Baloch 17
Complications: -
 Brain stem herniation.
 Brain death.
 Syndrome of inappropriate antidiuretic syndrome.
 Dehydration due to vomiting.
 Diabetes insipidus.
Diagnostic Care: -
 Clinical findings.
 Cerebral Angiography.
 C.T scan.
 L.P.
 M.R.I.
Nursing Care: -
 Assess the patient for bradycardia and increased blood pressure, which are initial features of
I.I.C.P.
 Elevation of the head of the bed to 30 degree with head in a neutral position to reduce the
cerebral edema.
 Extreme rotation of the neck and flexion of the neck are avoided because compression of
jugular vein cause increased intra cranial pressure.
 Emotional stress should be avoided because these conditions may cause alteration in brain.
 Abdominal distention, which increases intra cranial pressure should be noted.
 Clearance of the airway should be done.
 Control the coughing if it is in severe condition.
 Maintain the fluid balance.
 Manage the potential complications.
Unconsciousness
Unconsciousness is an abnormal state in which the patient is unknown of self or environment.
Level of consciousness: -
Alert  Confused  Lethargic  Obtunded  Stoporous  Comatose.
Alert: -
Attends to environment, responds appropriate to commons and questions with minimal stimulation.
Confused: -
Disoriented to surrounding, may have impaired judgment.
Lethargic: -
Drowsy, need gentle verbal or touch stimulation to initiate response.
Obtunded: -
Response slowly to external stimulation, needs repeated stimulation to maintain attention.
Stupurous: -
Responds only minimally with vigorous stimulation, may only mutter.
Comatose: -
No verbal response to any external stimuli.
Components of Consciousness: -
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- Arousal: - Function of brain stem pathways that govern wakefulness. Particularly the
reticular activating system.
- Content: - Refers to ability to reason, think and to react to stimuli with purpose and
awareness contents include behavior, thought, language and expression.
Glasgow Coma Scale: -
Category & Response : Score
1. Eye opening: -
- Spontaneous movement 04
- Open to verbal request 03
- Open with painful stimuli 02
- No opening 01
2. Best verbal response: -
- Orient to person, place & time & 05
converse appropriately.
- Converse but confused 04
- Words spoken but word (conversation 03
not sustain).
- Sound made, no untellable words. 02
- No response. 01
3. Best Motor Response: -
- Obeys command. 06
- Localize to painful stimuli 05
- Withdraws to painful stimuli 04
- Abnormal flexion to pain (decorticate posture) 03
- Abnormal extension to pain (decerebrate 02
posturing)
- No response 01
Causes: -
 Trauma
 Intra cranial hemorrhage.
 Hematoma
 Cerebral edema.
 Cerebral infarction.
 Meningitis.
 Encephalitis.
 Cerebral abscess.
 Neoplasm.
 Hypoglycemia.
 Diabetic Ketoaccidosis.
 Uremia.
 Hepatoencephalopathy
 C.S.F
 Poisoning.
 Heat stroke.
Sakhawat Baloch 19
 Decreased wakefulness.
 Decreased attention to environment.
 Confusion.
 Disorientation.
 Poor memory.
 Decrease mobility.
 Less or no response to stimuli.
Complications: -
 Respiratory failure.
 Pneumonia.
 Pressure ulcer.
 Aspiration of gastric contents.
 Hypoventilation.
Management: -
Medical management depends on the cause.
Nursing Care: -
 Turn the side-to-side four hourly.
 Encourage coughing and deep breathing while awake.
 Suction oral and pharyngeal airway.
 Monitor oxygen saturation and blood gases.
 Maintain hydration, prevent hypovolumia.
 Promote tissue perfusion.
 Perform passive and active range of motion.
 Orient patient to surrounding.
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Intracranial Tumor
Brain Tumor: -
Abnormal new growth in brain tissue is called brain tumor. It may be benign or malignant in nature.
Intracranial Tumor: -
Tumors of the brain may be primary: arising with in the brain or secondary: resulting from a metastasis
from malignant neoplasm else where in the body. Brain tumors are classified into types according to
the tissue from which they arise.
Types: -
1. Gliomas.
a) Astrocytoma.
b) Glioblastoma.
c) Oligodendroglioma.
d) Medulloblastoma.
2. Meningoma.
3. Pituitary adenoma.
4. Metastatic cancer.
A) Gliomas: A tumor composed of neuralgia in any of its states of development.
a) Astrocytoma: - Arises from supportive tissue, glial cell and astrocytes. Usual location is the
white matter of the frontal and temporal lobes of adult.
b) Glioblastoma: - Arises from primitive stem cell, usually location is in cerebral hemispheres.
c) Oligodendroglioma: - Arise from glial cells and dendrites.
d) Medulloblastoma: - Arise from supportive tissue usually at posterior fossa, fourth ventricle. They
may be malignant.
B) Meningioma: - Arises from endothelial cell, fibrous tissue, usual location is arachnoid’s villi
dura.
C) Pituitary adenoma: - Arise from pituitary glandular tissue located at pituitary gland.
D) Metastatic tumor: - Spread of cancer cell from other organs such as lungs, breast, kidney,
thyroid etc….
Pathophysiology: -
The clinical manifestations of intra cranial tumors are generally caused by local destructive effects of
tumors, the resulting accumulation of metabolites, the displacement of the structure, obstruction of the
C.S.F and the effects of edema and increased intra cranial pressure.
 “Pressure” Headache.
 Nausea and vomiting unrelated to food intake.
 Symptoms of increased intracranial pressure.
 An antiseptic shampoo may be ordered before surgery.
 Make sure that all the requirements such as consent etc are completed.
 blurred vision.
 Altered level of consciousness.
 If cerebral hemispheres is involved.
 Hemiplegia, seizures, memory defect, ataxia gait, speech disturbance, Asphasia
Sakhawat Baloch 21
 x-ray.
 MRI
 EEG
 L.P
 CT scan..
Management: -
 Phenytoin is used to control seizure.
 Dexamethasone to relieve edema.
 Laxatives as stool softener. Surgery, these include Burrhole, Carniotomy, Carnioplasty,
Shunt procedure
Post Operative Care: -

1. Performing monitoring
2. Assess neurological status.
3. Assess degree and character of drainage.
4. Observe the dressing.
5. Observe for leakage of C.S.F.
6. Promote decreased intracranial pressure.
7. Coughing and vomiting should be controlled and their occurrence should be fully
controlled.
8. Maintain proper position of patient.
9. Assess the sign & symptoms of increased intracranial pressure.
10. Promote electrolytes balance.
11. Promote comfort.
Pre-operative Care: -
 Base line data of neurological and physiological status record.
 Patient and his family are encouraged to verbalize.
 Treatment and procedure explained fully to patient.
 If head is to be shaved, it is usually done in O.T.
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Migraine
This is symptom complex characterized by periodic and recurrent attacks of severe headache. The
cause of migraine has not been clearly demonstrated but it is vascular disturbance occurs more
commonly in women and has strong familial tendency.
It is also can be defined as” lateralized throbbing headache that occurs episodically.
Physiologically, the migraine headache is a neurological condition more common to women than to
men. The French word migraine derives from the Greek hemicrania (half skull) and the Old English
megrim (severe headache).
Pathophysiology: -
The signs and symptoms of migraine result due to cortical Ischemia. The typical attack begins with
vasoconstriction affecting the arteries of the scalp and cerebral arteries. Extra cranial and intracranial
blood vessels than dilate causing pain and discomfort. Studies suggest that dilated arteries become
hyper permeable and local inflammatory reaction occurs in painful dilated arteries. It is proposed that
vasoactive substance histamine, serotonin, participate in the inflammatory reaction.
Causes of Migraine: -
1. Stress.
2. Excessive sleep.
3. Lack of sleep.
4. Familial history.
5. Menstruation.
6. Constipation.
7. Alcohol.
8. Oral contraceptive.
9. Vascular disorder.
10. Stress.
A. Aura phase:
 Lasts up to 30 minutes.
 Visual disturbance
 Dizziness
 Light flashes.
 Tingling on the face.
 Mild confusion.
 Slight weakness.
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B. Headache Phase:
 Lateralize dull, throbbing pain.
 Photophobia.
 Nausea & vomiting.
 Pulsation of external carotid artery.
 Stars, sparks unformed light flashes.(luminous hallucination)
 Duration of this period ranges from hours to days.
C. Recovery Phase:
 in this phase patient feels well.
Diagnostic criteria:
A. At least five attacks fulfilling criteria B-D
B. Headache attacks lasting 4-72 hours [when untreated]
C. Headache has at least two of the following characteristics:
1. Unilateral location
2. Pulsating quality
3. Moderate or severe pain intensity
4. Aggravation by or causing avoidance of routine physical activity
D. During the headache at least one of the following:

1. Nausea and/or vomiting
2. Photophobia and photophobia
Management:-
Rx.
Cafergot (migril) : one tablet as soon as after attack , repeat if necessary.
Nursing Care:-
 A migraine headache in the early phase requires abortive drug therapy.
 Nursing care during a fully developed attack includes comfort measure such as quite, dark
environment.
 Stress is believed to be a factor in the precipitation of migraine.
 Instruction about the importance of proper diet, adequate rest and coping strategies may
help the patient to deal with stress.
 Long intervals between meals also should be avoided.
 Women should avoid oral contraceptive.
 Proper rest should be advised.
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Cerbro-Vascular Accident or Stroke
A stroke is the rapidly developing loss of brain functions due to a disturbance in the blood vessels
supplying blood to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis
or embolism or due to a hemorrhage. As a result, the affected area of the brain is unable to function,
leading to inability to move one or more limbs on one side of the body, inability to understand or
formulate speech or inability to see one side of the visual field
Classification
Ischemic stroke
In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain
tissue in that area. There are four reasons why this might happen: thrombosis (obstruction of a blood
vessel by a blood clot forming locally), embolism (idem due to an embolus from elsewhere in the
body,) systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[6] and venous
thrombosis.
Hemorrhagic stroke
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is
made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood
inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage
or intravascular hemorrhage (blood in the vescularcular system).
.Causes of stroke :-
1. Arteriosclerosis & thrombus formation: -
Cerebral arteriosclerosis are major cause of cerebral thrombosis which is the most common
cause of stroke.
2. Cerebral embolism: -
Pathologic abnormalities from myocardial infection or muscloskeletal embolus formation may
cause C.V.A.
3. Cerebral Ischaemia: -
Caused by cerebral athermanous constriction of arteries.
4. Cerebral Hemorrhage: -
 subdural hamorrhage.
 Subarachnoid hemorrhage.
 Intracerebral hemorrhage.
These hemorrhages are caused by skull fracture due to trauma/ accidents or hypertension.
Risk Factors: -
1. Hypertension.
2. cardiovascular disease.
3. elevated cholesterol in blood.
4. obesity
5. Diabetes mellitus.
6. Smoking.
7. oral contraceptives.
8. Fractures.
Sakhawat Baloch 25
Pathophysiology: -
Cerebral blood flow is maintained at 750 ml/minute. About 20% of the flow to the brain ensures the
optimal cerebral function. If this is interrupted due to any cause may cause C.V.A. neurologic
metabolism is altered in 30 seconds, metabolism stop in 2 minutes and cellular death occurs in 5
minutes after interrupted blood flow. The interruption of blood occurs due to many cause, these causes
are cerebral Ischaemia and signs and symptoms appear due to neurological defect.
 Motor loss
 Hemiplegia (paralysis of one side of body).
 Hemiparesis (weakness of half body).
 Atexia ( unsteady gait, unable to keep feet together).
 Dysarthia ( difficulty in forming words).
 Dysphagia ( difficulty in swallowing).
 Paresthsia ( numbness, tingling in body).
 Expressive aphasia ( unable to form words).
 Receptive aphasia ( unable to comprehene spoken words)
 Loss of control.
 Hemianopsia ( unable to see)/
 Bladder incontinence.
 Loss of peripheral vision.
 Decrease tolerance.
 Altered judgment.
 Altered / no perception.
 Involvement vertebral basilar
 Artery causes involvement of all $ extremities.
Investigations: -
 C.T scan.
 C.S.F analysis.
 E.E.G
 M.R.I.
 Angiography.
Sakhawat Baloch 26
Complications: -
 Cerebral hypoxia.
 Brain tissue death.
 Cerebral embolism.
Rx:-
 I / V Heparin.
 B1, B6, B12 ( Neurobian ).
 Antibiotic therapy.
 Barbiturates.
 Removal of cause e.g. Hypertension, thrombus etc..
Nursing Care: -
 Monitor cerebral perfusion by assessing mental status.
 Prevention of complications of immobility and disease by proper positioning, complication
may occur such as contraction & skin break down.
 Prevent shoulder adduction by placing pillow in axilla.
 Change the position every 24 hourly.
 Exercise of the effected extremities.
 For preventing the hip rotation place a sand bag at the side of legs, which prevents external
rotation.
 Help the patient for achieving self care.
 Monitor skin integrity.
 Improve family coping through health teaching.
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Gullain-Barre’s Syndrome
This is an inflammation of the polyneurons characterized by varying degree of motor weakness or

paralysis. It primarily affects the motor system of cranial and spinal nerve and results in the loss of
myelin (segmental demyeliation) and edema and this inflammation of effected nerve causing a loss of
neurotransmission to the periphery.
Causes: -
It is believed that cell mediated immunological reaction directed at the peripheral nerve. The syndrome
may also be produced by immune system stimulation from a viral infection, trauma, surgery, H.I.V
infection etc. These conditions/stimuli are thought to cause an alteration in immune system resulting in
sensitization of T.lymphocytes to the patient’s myelin causing myelin damage.
Pathophysiology: -
In Gullain-Barre’s Syndrome an immune mediated response triggers. The destruction of the myelin
sheath surrounding the peripheral nerve, nerve foot, root ganglia and spinal cord. Collection of
lymphocytes and macrophages are believed to be responsible for stripping demyelination causes
blocked stimuli from node to node.
Sings and Symptoms: -
1. Ascending G.B.S: - This is most common form. In this weakness, numbness and paralysis
begins in the legs and progress upward.
2. Pure/motor G.B.S: -Similar to ascending but in this there is no sensory involvement.
3. Descending G.B.S: - In this weakness in the muscle controlled by cranial nerve and then
progress downward.
Complications: -
1. Respiratory Failure
2. Pulmonary emboli
3. Paralytic ileus
4. Nutritional
5. Hypotension
6. Muscle atrophy.
Management: -
Carticosteroid to reduce autoimmune inflammation.
Nursing Care: -
 Assess the respiratory function
 Prepare the patient for mechanical ventilation.
 Maintain optimal body alignment
 Assess airway potency
 Maintain the hydration
 Assess the difficulty in speaking
 Reassure the patient
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Musculo-Skeletal Disorders
Muscular System: -
Muscles are involved in body movement, posture and heat production function. The muscles
are attached by tendons or flat sheet of connective tissue to bone, connective tissue, other
muscles, soft tissue and skin. Muscles vary in size and shape according to their activity.
Muscles of body are composed of parallel groups of muscle cells called Fasciculi encased in
fibrous tissue called epimysium.
Myoglobin is hemoglobin like protein pigment that is present in striated muscle cells. It
transport oxygen for the cells metabolism. Each muscle cell contain myofibrils, composed of
series of Sarcomere; the actual contractile unit of skeletal muscles. Sarcomere is composed of
thin and thick filament Thin filaments are composed of protein called actin & Thick is
composed of myosin.
Skeletal Muscles: -
Contraction of a muscle is due to contraction of each of its component Sarcomere. The
contraction is due to interaction between myosin in thick filament and action acticin in this
filament. Thick and thin filaments slide across one another. when calcium level in sarcomere
falls the myosin and actin fail to interact and sarcomere turns to its original length. Actin and
myosin do not interact in the absence of calcium.
Depolarization normally occurs in the response to stimulus delivered by nerve cell.
The communication between nerve cell and muscle cell takes place at motor end plate. The
neurons that control the activity of muscles are called motor neurons originate in anterior horn
of spinal cord. For muscle contraction energy is required source of energy is A.T.P.
Types Of Muscle Contraction: -
Isometric Isotonic
In this length of muscle remains Contraction of muscles
constant but force generated by characterized by the shortening
muscle is increased. E.g. pushing of muscles with no increase in
against immoveable wall. tension in muscles e.g. walking
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Muscle Tone: -
Relaxed muscles demonstrate a state readiness to respond to stimuli. This state of readiness is
called tonus (tone). Muscle that has less tone is called flaccid & muscle with more tone is
called spastic. Absence of tone is called atonic.
SOME TERMS: -
1. Scoliosis: -
Lateral curving deviation of spine.
2. Kyphosis: -
An increased roundness of the thoracic spine curve.
3. Lordosis: -
Sway back, exaggeration of the lumber spine curve.
4. Contracture: -
Shortening of surrounding joint structure.
5. Dislocation: -
Complete separation of the joint structure.
6. Flexion: -
Bending at joint.
7. Extension: -
Strengthening at joint.
8. Abduction: -
Action of moving away from midline of body.
9. Adduction: -
Action of moving towards the midline.
Physiology Of Musculo-Skeletal System

Bony structure and connective tissue accounts for approximately 25% of body weight and
muscles accounts for approximately 50%.
 The bony structure provides protection for vital organs e.g. brain, heart and lungs.
 Bony skeleton also provides framework to support the body structure.
 Muscles attached to bones help in movement.
 The matrix of bone stores calcium, phosphorus, magnesium etc. About 99% of total
calcium is present in bones.
 The bone marrow in bone synthesis of WBCs, RBCs and Platelets.
Anatomy Of The Skeleton System: -
There are 206 bone in human body divided into four categories 1. Long Bones (femur) 2. Short
Bones (tarsal) 3. Flat Bones 4. Irregular Bones (vertebrae).
Bones are constructed of cancellous (spongy) or cortical (compact) tissue long bones such as
femur consist of diaphysis and epiphysis (lower and upper extremities).
Bone is composed of 1. Cells 2. Protein matrix 3. Mineral deposits.
There are three bones cells 1. Osteoblast 2. Osteocytes 3. and Osteoclast.
Osteoblasts: function is bone formation by secreting matrix; matrix is framework in which
inorganic salts are deposit.
Sakhawat Baloch 30
Osteocytes: Acts as bone maintenance.
Osteoclast: It function as bone destruction, remodeling of bone.
Osteon: -
It is microscopic functioning unit of mature bone. The center of osteon contains capillaries.
Around the capillaries the circles of bone matrix are present which contains osteocytes.
Covering of bone is called periosteum which nourish the bone, allows for growth and provides
area for the attachment of tendon & ligament. The endsteum is thin membrane covering the
marrow cavity.
Bone Formation: -
Bone begins to form long before birth. Ossification is the process by which the bone matrix is
formed and hardening minerals. There are 2 modes of ossification.
1. Intramembranous Ossification: -
Ossification that occurs in and replaces connective tissue.
2. Endochondral Ossification: -
In this cartilage model exist cartilage like osteiod is formed, resorbed and replaced by bone.
Most bones in body are formed and heal by endochondral ossification.
Bone Maintenance: -
Bone is maintained by reabsorption and absorption. In this hormones are involved in these
process such as paratharoxone, calcitonin, oestrogen, progesterone etc.
Bone Healing: -
1. Inflammation:
There is bleeding in the injured tissue and formation of fracture hematoma. The injured area is
invaded by macrophages which debride the area.
2. Cellular Proliferation:
Within 5 days fibrin threads form within clot creating network revascularization. Fibroblast
and osteoclast produce collagen for collagen matrix at the fractured area.
3. Callus Formation:
Tissue growth continues and the cartilage collar each bone fragment grows towards the other
until the gap is bridged. The fractured fragments are joined by fibrous tissue, cartilage and
immature bone fiber. It takes 3-4 weeks for fractured fragments to be united by cartilage.
4. Ossification:
The developed callus begins to ossify through process of endochondrial ossification. Minerals
are continuously deposited until bone becomes firm. Long bones take 3-4 months for
ossification.
5. Remodeling:
In this final stage remaining devitalized tissue are removed and recognizing the new bone into
its former structural arrangement. It may takes months to years depend on the bone
Sakhawat Baloch 31
Management Of The Patient In a Cast
Cast: -
This is rigid external immobilizing device that is molded to the counters of the body to which it
is applied.
Purpose: -
 To immobilize the part in a specific position.
 To apply uniform pressure on encased soft tissue.
 To correct the deformity.
 To provide support and stability for weakened joint.
Types: -
1. Short Arm Cast:
It extends from below the elbow to the palmer crease, secured around the base of thumb. If
thumb is used it is called thumb spica or gauntlet “thumb”
2. Long Arm Cast:
Extends from upper level of axillary’s fold to the proximal palmer crease. Elbow is usually
immobilized at right angle.
3. Short Leg Cast:
Extends from below the knee to the base of the toe.
4. Long Leg Cast:
From upper and middle third of thigh to the base of toe. Knee joint is slightly flexed.
5. Body Cast:
Encircle the trunk.
6. Spica Cast:
Incorporate the portion of trunk and one or two extremities.
7. Shoulder Spica Cast:
A body jacket that enclosed trunk and shoulder and elbow.
8. Hip Spica Cast:
Enclosed trunk and lower extremity.
Nursing Care Of Patient With Cast: -
1. Assess the cast and remaining area.
2. Evaluate for pain, if occur, indicate skin break down, more pressure, pressure ulcer
etc. most pain can be relieved by elevating the involved area, applying cold as
possible and with analgesics.
3. Unrelieved pain must be reported immediately to the doctor to avoid possible
necrosis and paralysis.
4. Every joint that is not immobilized must be excursed or move through range of
motion.
5. Assess for bluish colour of extremities.
6. Provide firm mattress on bed.
7. Change the position 2 hourly.
8. Maintain adequate tissue perfusion.
Sakhawat Baloch 32
9. Patient education at Home for Cast Management:

a) Move about as normally as possible.
b) Avoid excessive use of injured extremity.
c) Perform the prescribed exercise regularly.
d) Elevated the casted extremity at heart level.
e) Keep the cast dry.
f) Don’t cover the cast with plastic or rubber.
g) Avoid walking on wet, slippery floors.
h) Cushion rough edges of cast with tape.
i) Remove the surface soil with damp clean cloth.
j) Don’t scratch the skin under the cast.
k) Note odor about the cast if present report to health personnel.
Complications Of Cast: -
1. Pressure ulcer
2. Cast syndrome
3. Impaired blood flow to lower to cast.
4. Cyanosis to affected part.
5. Paraethesis.
Managing The Patient In Traction
Traction:
Traction is the application of a pulling force to a part of the body to minimize muscle spasm
and maintain the position of effected part.
Purpose:
 To minimize the muscle spasm.
 To immobilized the body part.
 To reduce and align the fractures
 To reduce the risk of deformity.
 To treat the dislocation.
 To attain equilibrium.
Principles of Effective Traction:
Whenever traction is applied the counteraction must be considered. Counteraction is the force
that acts in the opposite direction (Newton’s 3rd law). Patient’s body weight and bed position
adjustment supply the needed counteraction.
 Any factor that reduces the pull, must be eliminated.
 Patient is in good body alignment in the center of bed when traction is applied.
 Ropes must be unobstructed.
 Weights must hang freely not rest on bed or floor.
 Knots of rope must not touch the pully.
Sakhawat Baloch 33
Types: -
1. Straight Or Running Traction:
Applies force in a straight line with the body rest on the bed e.g. Buck’s extension traction and
pelvic traction are best examples.
2. Balance Suspansion Traction:
Support the body part of the bed.
3. Skin Traction:
Traction applies to skin.
4. Skeletal Traction:
Applies to skeleton.
Potential Complications:
 Pressure ulcer
 Lung congestion & pneumonia.
 Constipation
 Urinary stasis & infection
 Deep vein thrombosis
 Swelling
 Discomfort in calf muscles.
Weight Applied:
Skin Traction Skeletal Traction
Not more than 2-3 kg (4.5-7lbs) 7-12 kg (15-25 lbs)
Nursing
but pelvic traction is 4.5-9 kg
(10-20 lbs) Care:
 Assess the patients neurovascular status.

 Ensure that effective traction is maintained e.g. rope and pully are freely moveable,
prescribed weight hangs freely.
 Ensure that patient is in correct position.
 Maintain the continuous traction unless otherwise prescribed.
 Reposition within therapeutic limits.
 Involve the patient in care to reduce anxiety and depression.
 Encourage for exercise.
 Observe skin break down.
 Observe pressure under sling & equipment.
 Monitor pain areas and provide skin care.
 Assess the signs & symptoms to complications.
Sakhawat Baloch 34
Fractures
The break down in the continuity of the bone mainly occurs when the bone is subjected to
stress which it can not bear. The highest incidence of fracture is seen in male 15-24 years old
and in elderly women aged 65 years or more.
Causes:
1. Crushing force.
2. Accident
3. Twisting motion.
4. Extreme muscular contraction.
5. Osteoporosis etc.
Types:
1. Complete Fracture:
Fracture involves a break occurs the entire cross section of the bone and is frequently displaced
(remove from normal position).
2. Incomplete Fracture:
The break occurs through only part of the cross section of the bone.
3. Closed Fracture/Simple Fracture:
Fracture does not produce break in skin.
4. Open Fracture/Compound Fracture:
Type of fracture in which skin & mucus membrane wound extends to the fractured bone. Open
fracture is graded on Grade I= Clean wound less than 1 cm Grade II= Large wound without
extensive soft tissue damage Grade III= Highly contaminated wound with damage of soft
tissue.
Other Specific Types are:
1. Green Stick: fracture and in which one side of bone is broken and other side is bent.
2. Transverse: Fracture that is straight across the bone.
3. Oblique: Fracture that occurs at an angle across the bone.
4. Spiral: Fracture twisting around the shaft of the bone
5. Communited: Fracture in which bone is broken unto several fragments.
6. Depressed: Bone fragments are driven inward (e.g. in skull and facial bone)
7. Epiphyoeal: Fracture through the epiphyseal.
8. Impacted: Fracture in which bone fragment is driven into an other bone fragment.
9. Pathological: Fracture of diseased bone e.g. osteoporosis, peget’s disease.
10. Avulsion: Fracture of bone that occurs due to the pull of the tendon or ligameny.
Clinical Features:
1. Severe pain, which is continuous until bone is immobilized
2. False or unnatural motion .
3. Deformity
4. Shortening of extremity.
5. Grating sensation when touched (crepitus).
6. Localized swelling & edema.
7. Skin discoloration.
Sakhawat Baloch 35
Emergency Management:
When fracture is suspected it is most important to immobilize that body part immediately
before patient is moved to hospital.
If patient is removed from vehicle before splint can be applied, the extremity is supported
above & below the fractured site to prevent rotation as well movement of effected part.
The pain is severe, it can be relieved by preventing movement of fractured part.
Appropriate splint are essential to prevent tissue damage.
The injured area can be immobilized by applying temporary well padded splint, which then
bandage firmly.
In open fracture cover the wound with clean sterile dressing to prevent contamination.
No attempt is made to reduce the fracture, even if fragment protrude from injury.
Patient’s clothes may be cut away from site and is fracture is reduced by trained surgeon in
O.T.
Principles Of Managing Fracture:
1. Fracture Reduction:
Reduction of fracture (“setting the bone”) refers to restoration of the fracture fragments into the
anatomic alignment and rotation.
In closed reduction bone fragments are brought into apposition(ends in contact) by
manipulating and manual traction.
Open reduction requires open surgery internal fixation devices in the form of metallic pins,
wires, screw, slates, nails or rods may be used to hold the bone fragments in the position.
2. Fracture Immobilization:
After fracture reduction bone fragments must be immobilized or held in correct position.
Immobilized bone may be accomplished by external or internal fixation. External fixation
include cast, splint, bandage etc.
3. Maintaining The Function:
Efforts should be taken to maintain the function.
4. Restoring The Function:
Assessment for neurovascular status. Involvement of patient in self-care etc
Sakhawat Baloch 36
Facture Effecting Fracture Healing:
A. Factors Enhancing Fracture Healing:

 Immobilization of fracture fragments.
 Maximum bone fragment contac.
 Sufficient blood supply.
 Proper nutrition.
 Hormones growth hormones, calcitonin etc.
B. Factors Inhibiting Fracture Healing:

 Extensive local trauma.
 Bone loss
 Inadequate immobilization.
 Space between bone fragment.
 Infection.
 Local malignancy.
 Metabolic bone disease.
 Vascular necrosis.
 Old age
 Corticosteroid
Time Necessary For Union Of Bones:

- Phalanx (finger) 3-5 weeks - Metacarpal 6 weeks
- Carpal 6 weeks - Radius & Ulna 10-12 weeks
- Humerus 8-12 weeks - Clavicle 6-10 weeks
- Vertebrae 16 weeks - Pelvis 16 weeks
- Femur 18-24 weeks - Tibia 14-20 weeks
- Calcaneus 12-16 weeks - Metacarpal 6 weeks
- Phalanx (toe) 3 weeks
Complications Of Fracture:
 Shock
 Embolism.
 Compartment syndrome.
 Permanent loss of extremity.
 Infection
 Thromboembolism
Sakhawat Baloch 37
Contusions strains& sprains
Contusion:
This is an injury of the soft tissue produced by the blunt force (e.g. a kick, fall etc). The
resultant rupture of many vessels lead to bleeding into soft tissue ( Ecchymosis, bruising). The
local symptoms are pain, swelling and discoloration. Most of them are resolve in 1-2 weeks.
Strain:
This is muscle pull due to over use, over stretching or excessive stress. Patient experience local
tenderness upon the muscle use and isometeric contraction.
Sprain:
It is an injury to ligamentous structured surrounding the joint caused by twisting motion. The
joint becomes tender and movement is limited. .
Treatment of contusion, sprain & strain consists of resting and elevation of effected part and
applying cold and using a compression bandage. Cold should be applied intermittently for 20-
30 minutes during first 24-48 hours. Cast is necessary if joint is unable to perform function.
After 48 hours injury heat may be applied to reduce muscle spasm and promote vasodilation,
absorption & repair.
Excessive exercise should be avoided, these may lead to severe tissue damage. Strain & sprain
may take weeks to months for healing.
Painkiller may be used to reduce pain, swelling etc.
Antibiotic may be used to prevent from secondary infection.
Joint Dislocation:
A dislocation of a joint is a condition in which the articular surface of the bones forming the
joint are no longer in anatomic contact. The bones are literally “out of joint”.
Dislocation may be congenital (present at birth), spontaneous (pathologic) & traumatic.
The signs and symptoms are pain, change in conteur of joint, change in length of extremity,
loss of normal mobility. X-rays confirm the diagnose.
Management:
 The affected joint needs immobilization.
 The dislocation is reduced (i.e. displaced parts are brought in normal position).
 The head of dislocated bone is brought on the cavity of other bone.
 The joint is immobilized by splint or cast.
 Analgesic to control the pain
 Antibiotic to control any infection etc.
Sakhawat Baloch 38
Osteomyelitis
Osteomyelitis is an infection of bone by direct or indirect invasion of an organism. Bone infection is

more difficult to cure than soft tissue infection due to limited blood supply. The inflammation causes
increased tissue pressure involucrum formation. According to the entry of the pathogenic
microorganism into two types.
1. Exogenous Osteomyelitis.
2. Endogenous Osteomyelitis.
1. Exogenous Osteomyelitis:
It is secondary to contagious source of infection, that is caused by a pathogen from outside the body
e.g. infection from an open fracture or surgical procedure, involving instrumentation and animal bite.
The most common organism cause exogenous osteomyelitis is staphylococci.
2. Endogenous Osteomyelitis:
It is caused by blood bone pathogen originating from infection site with in body. In hematogenous
osteomyelitis the infection spread from bone to soft tissue and skin. The most common organism is
staphylococci aureus.
Pathophysiology:
Staphylococcus aurues causes 70-80% of bone infection.
The onset of osteomyelitis after orthopedic surgery may occur during the first three months is called
Acute Fulminating (stage I) Delay onset (stage II) infection occur between 4-24 months and late
onset (stage III) osteomyelitis occers 2 or more years after surgery.
The initial response to infection is inflammation, edema and increased vascularity. After 2-3 days
thrombosis of the blood vessels occurs in the area resulting ischaemia with bone necrosis. The
infection extends to medullary cavity and under the peristeum and may spread to adjacent soft tissue
and joints is resulting abscess cavity, has in its walls areas of dead tissue, as in any abscess cavity. The
dead bone tissue does not easily liquefy and drain. New bone growth (Involucrum) forms & surrounds
sequestrum (dead bone tissue).
Clinical Features:
 High fever & chill
 Pain in effected area
 Swelling at the effected area
 Pulsation pain
 The pain intensifies with movement and movement due to pressure of collecting pus.
 The local (effected) area remain red and tender.
Management:
 Antibiotic therapy according to pus culture.
 Calcium supplement with vitamin D
 Analgesic
 Surgical drainage of pus.
 Pain relieving procedure such as splinting to decrease the pain and muscle spasm.
 Elevations of extremities reduce the swelling & pain.
 Controlling infection process.
 Educate the patient for home care
Sakhawat Baloch 39
PAGET’S DISEASE (OSTEITIS DEFORMAN)
Paget's disease, also known as osteitis deformans, is a chronic disorder that typically
results in enlarged and deformed bones. It is named after Sir James Paget, the British
surgeon who first described this disease the excessive breakdown and formation of bone
tissue that occurs with Paget's disease can cause bone to weaken, resulting in bone pain,
arthritis, deformities, and fractures.
This is localized increase bone remodeling most commonly affecting the skull, femur,
tibia, pelvis bone and also vertebrae. There is primarily resorption of the bone followed
by compensatory increased in osteoblast activity (bone repair). The bone formed is high
in mineral content but poorly constructed. The bones are weak and pathological
fractures occur. Frequently the bone bow. This is genetically occurring in patients.
 Cortical thickness
 Enlarged head Skull may be thickened and complains hat no longer fits.
 Femur and tibia tend to bow.
 Chin rests on chest.
 Arms are bent outward & forward.
 Pain and tenderness in bone.
 Skin may be hot.
 Bone pain (may be severe and persistent)
 Bowing of the legs and other visible deformities
Diagnosis
 Pagetic bone has a characteristic appearance on x-rays. A skeletal survey is

therefore indicated.
 An elevated level of alkaline phosphatase in the blood in combination with
normal calcium, phosphate, and aminotransferase levels in an elderly patient are
suggestive of Paget's disease.
 Bone scans are useful in determining the extent and activity of the condition. If a
bone scan suggests Paget's disease, the affected bone(s) should be x-rayed to
confirm the diagnosis.
Sakhawat Baloch 40
Diet and Exercise
In general, patients with Paget's disease should receive 1000-1500 mg of calcium,

adequate sunshine, and at least 400 units of vitamin D daily. This is especially important
in patients being treated with bisphosphonates. Patients with a history of kidney stones
should discuss calcium and vitamin D intake with their physician.
Exercise is very important in maintaining skeletal health, avoiding weight gain, and
maintaining joint mobility. Since undue stress on affected bones should be avoided,
patients should discuss any exercise program with their physician before beginning
Management: -
Usually no treatment is recommended for the patient without symptoms.
GAS GANGRANE
This is severe infection of skeletal muscles usually caused by clostridium species. The
anaerobic organism clostridium perfringens, clostridium septicum grow easily in wounds.
 Sudden severe pain occurring 1-4 days following injury.
 Darkened skin.
 Vesicles filled with serous fluid.
 Foul smelling from fluid.
 Involved muscle become necrosis.
Management: -
 Surgical debridment is best treatment.
 Amputation of effected part is necessary.
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RHEMUTOID ARTHRITIS
Rheumatoid arthritis is a chronic inflammatory disease characterized by recurrent

inflammation of connective tissue.
Causes & pathophysiology: -

There are three causes:
1. Infection
2. Autoimmune
3. Genetic facter.
The genetic predisposition has been identified related to certain human leukocytes
antigen(HLA) called HLA Dr4. The antigen stimulus such as virus leads to formation of an
abnormal immunoglobin “a” “IgG” Rheumatoid arthritis is characterized by presence of
antibodies against this abnormal “IgG”. The antibodies to this altered IgG is called rheumatoid
factor and they combine with IgG to form immune complex that deposits in the joint blood and
pleura complement is activated & an inflammatory response occur.
Actually disease begins with in joint. The infiltrating macrophages are activated and release
variety of cytokinese in interleukin 1 & interleukin 6. These enzymes again damage the
membrane and damage the bone and cartilage.
It can be explained by four stages.

Stage 1: -
Unknown etiological factors initiate joint inflammation synovitis& produce excessive fluid.
Stage 2: -
Panel (inflammatory granular tissue) is formed at the junction of the joint. This extends over
the surface of articular cartilage and eventually incades the joint capsule and bubchondria
bone.
Stage 3: -
Fibrous connective tissue replace the granular tissue and occluding the joint space. Fibrous
ankylosis results in decreased joint motion.
Stage 4: -
A fibrous tissue calcifies, bony ankylosis may result and cause total joint immobilization.
 Morning stiffness
 Pain at rest and during movement
 Bilateral joints are effected
 Frequently small joints are involved e.g. fingers proximal metacarpal joints.
 Paresthesia
 Contractures (flexion)
Sakhawat Baloch 42
Diagnosis: -
Positive Rh facter
Management: -
 NSAIDs and cartisone
 Stabilizing and supporting the joint
 Protect the joint from external trauma
 Assist patient to exercise in the specific joint
 Electric heating to provide extra warmth
 Maintain the muscle tone by range of motion
 Use assistive device if indicated
GOUT/GOUTY ARTHRITIS
This is heterogeneous group of conditions related to genetic defect characterized by hyper
urecemia, recurrent attack of arthritis. This is caused by either over secretion of uric and/or
impaired excretion of uric and through kidneys.
Pathophysiology:-
Hyper urecemia can cause urate crystals deposition. The attack of gravity arthritis is caused by
sudden increase or decrease of serum uric acid levels. When the urate crystal precipitate with
in a joint and inflammatory response occur and attack of gravity occur with repeated attack,
accumulation of sodium urate crystal called “Tophi” are deposited in peripheral part of body is
toes, hands etc.
Signs & Symptoms: -

 Involvement is usually manarticular often involve first metatarsal phalangeal joints
 Great toe is the most susceptible joint.
 Hip and shoulder are rarely involved.
 Distribution of the arthritis is usually asymmetrical.
 The involved joint is swollen, tender and over lying skin tension.
 Fever reach at 39 centigrade
 Elevated serum uric acid
Management: -
 Indomethacin
 Carticosteroid 40-60 mg/day
 Avoid meat, sea food, yeast, beverages, bear, alcohol, beans, peas, spinach,
cauliflower etc….
 Bed rest
 Avoid exercise, movement of the joints
 Instruct the patient to loose the weight.
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OSTEO ARTHRITIS OR DEGENERATIVE JOINT DISEASE
(DJA)
This is also called degenerative joint disorder. It is slowly progressive disorder of articulating
joint particular weight bearing joints and is characterized by degeneration of articular cartilage.
Causes: -
 Genetic disorder
 Metabolic disorder
 Previous trauma
 Fracture
 Infection.
Pathophysiology: -
It is generally termed as non-inflammatory or a small amount of low grade inflammation is
observed. In osteo arthritis, the articular cartilage is involved characterized by erosion of
articular cartilage, thickening of subchondrial bone and formation of bone spurs.
Degenerative change cause yellowness and opaqueness of white transparent joint thinner bony
surface or drawn together as the articular surface become totally denuded of cartilage, new
bone out growth is formed at joint margin and at the attachment sites of ligaments.
Signs and symptoms: -
 Joint pain and stiffness
 Limited range of motion
 Muscles spasm
 Reduce mobility
 Feeling grinding and catching in joint
 Hip involvement is common in man
 Knee involvement is common in woman.
Post operative Care Of Patient with total Hip Replacement:
1. Positioning: -
 Restriction is designed to avoid dislocation of the prosthesis.
 Flexion is limited to 60 degree for 6-7 days, then 90 degree for 2-3 months.
 No adduction is permitted beyond midline for 2-3 months
 No side lying on operated side
 No extreme external and internal rotation is permitted.
2. Wound Care: -
 Drains are inserted in wound to prevent formation of hematoma.
 Note amount and type of drainage.
 Use aseptic techniques
 Change dressing once daily.
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3. Activity: -
 Encourage periodic elevation and lowering the head of bed to provide motion at hip.
 Encourage active dorsiplanter flexion exercise of ankle and quadriceps and gluteal
setting exercise to promote venous return, prevent thrombus formation.
 Observe weight bearing restriction prescribed by surgeon.
 Increase amount of walking each day according to patient tolerance.
4. Medication: -
For controlling pain and healing.
5. Discharge Instruction: -
 Patient must use ambulatory aid.
 Avoid adduction.
 Limit hip flexion to 90 degree for 2-3 months.
 Patient must be made aware of the life long need for antibiotic prophylaxis.
Post Operative Care for Knee Replacement: -
1. Position: -
 The operative leg is elevated in pillow to enhance venous return for first 48 hours.
 Pillow are placed with caution not to flex knees.
 The patient may be turned from side to back to side.
2. Wound Care: -
 Drains are inserted in wound to prevent formation of hematoma.
 Note amount and type of drainage.
 Use aseptic techniques.
 Change dressing once daily.
 Assess the wound for smell and infection.
3. Activity: -
 Passive flexion in a machine with in prescribed flexion extension limits.
 Encourage to perform active dorsiplanter flexion of ankle, quadriceps setting.
 After the removing the drain straight leg rising exercise is prescribed.
 Partial weight bearing with an assistive device may be started and increased as
patient tolerated.
4. Medication: -
For pain control and other as prescribed by medical ifficer.
5. Discharge Instructions: -
 Patient must observe weight bearing restriction and use ambulatory aid for 2 months.
 Patient should continue active flexion and straight leg rising exercise.
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AMPUTATION
Amputation means removal of limb or its part or other appendages of body Amputation of lower
extremity is often necessary as a result of progressive peripheral vascular disease such as sequela of
diabetes Mellitus, gangrene, trauma, burns, electrical burns, malignant tumors. Of all these causes
peripheral vascular diseases account for majority of amputation of lower extremity. The major reasons
for upper extremity amputation are severe trauma, malignant tumor, infection, and gas gangrene.
The purposes of amputation are:
1. To relieve the symptoms.
2. To control the infection (gangrene).
3. To improve the function.
4. Save the patient’s quality of life.
Factors Effecting Amputation: -
 Age: -
Patient who require amputation are usually either young with severe extremity trauma or elderly with
peripheral vascular disease. The young are usually health and heal rapidly.
 Pathological condition of above:
e.g. osteoporosis.
 Chronic progressive disorders:
e.g. Diabetes Mellitus, Hypertension.
 Cardiovascular disorder.
 Respiratory disorder.
Level of Amputation
Amputation is performed at the most distal point that will heal successfully. Site of amputation
determined by two factors 1. Circulation in the part 2. Functional usefulness. The most appropriate site
for amputation are:
 Below the knees amputation.
 Above the knee amputation.
 Amputation of foot and ankle (Symes).
 Amputation of foot between metatarsus and tarsus (Hey’s).
 Hip disarticulation  removal of limb from hip joint.
Nursing Care: -
 Assess the amputation and monitor drainage for color and amount.
 Position of the patient with no flexion of hip or knee.
 Relieve the pain by administering of analgesic.
 Promote wound-healing strategies.
 Edema should be controlled by compression dressing.
 Give patient psychological support.
 Resolve grieving due to loss of extremity.
 Encourage for independent self care.
 Restore physical mobility.
 Encourage post operative exercise.
 Monitor for skin break down and potential complication.
Complications: -
 Phantom limb pain.
 Psychological stress.
 Bleeding.
 Infection.
 Impaired body image.
Sakhawat Baloch 46
Integumentary System
Assessment of the skin
Patient’s History: -
Patient describes his problem by health history. This provides primary cue/clue for further data
collection. The further information can be obtained by asking & observing:
 Skin Condition:-
Includes color, moisture, texture or integrity
 Onset: -
i.e. sudden or gradual
 Specific known cause: -
e.g. contact with poison or exposure to the allergen.
 Occupation: -
e.g. diseases such as contact dermatitis is seen in people who are in contact with chemical.
Physical Examination: -
Principles of physical assessment: -
1. Be Prepared: -
Includes private room for examination with moderate adequate room temperature & good
arrangement of light.
2. Be Systematic: -
i.e. from head to toe.
3. Be Thorough: -
Look at all the areas carefully, lift the folds of skin under breast or gluetal folds. Do not forget
to assess the mucus membrane.
4. Be Specific: -
When lesions are identified, observe for color, size & shape etc….
5. Compare the Symmetrical Part: -
Compare the right side with left side.
6. Record the Data: -
7. Use appropriate technique:
Color of skin
Pallor(Anemia)
Red Bluish Yellow
High fever Heat Hot flushes

Cyanosis Anxiety
Hemolysis Jaundice
Brown
Aging Acne Coritsone deficiency

Skin lesions: -
Sakhawat Baloch 47
There are two types of lesions:
1. Primary Lesions.
2. Secondary Lesions
1. Primary Lesions: -
These are original skin lesion arise from previously normal skin. These are the Primary Lesion:
1. Macula: -
Flat, non-palpable skin color change (color may be brown, white, red or purple). Macula are 1
cm with circumscribed border e.g. Mole, Petechia.
2. Patch: -
Also non-palpable skin with different colors. Patches are 1 cm may have irregular borders
e.g. freckles, echymosis.
3. Papule: -
Elevated palpable solid mass with circumscribed borders  0.5 cm with flat top e.g. warts.
4. Plaque: -
Elevated palpable solid mass, they may be coalesced. E.g. Psoriasis.
5. Nodule: -
0.5-2 cm, elevated, palpable, solid mass, extends deeper into the dermis than papule. E.g.
lipoma, squamous cell cancer.
6. Tumor: -
 2 cm, elevated, palpable, solid mass. Tumor do not always have sharp border e.g. large
lipoma, carcinoma.
7. Vesicle: -
Elevated palpable mass containing serous fluid,  0.5 cm e.g. herpes simplex, chicken pox,
small burn blisters.
8. Bulla: -
Elevated palpable mass  0.5 cm contains serous fluid e.g. large burn blisters, bullous
impetigo, both vesicle & bulla have circumscribed borders.
9. Pustules: -
Pus filled vesicles or bulla. E.g. Imptigo, furuncle, carbuncle.
10. Cyst: -
Encapsulated fluid filled or semisolid mass occurs in subcutaneous tissue or dermis. E.g.
sebaceous cyst, epidermoid cyst.
2. Secondary Lesions: -
Originate from the secondary lesions.
1. Erosion: -
Loss of superficial epidermis, does not extend to dermis seen as depressed moist area. E.g.
ruptured vesicle, scratch marks.
2. Ulcer: -
Skin loss extending to epidermis, necrotic tissue loss e.g. pressure ulcer.
3. Scale: -
Flakes, secondary to desquamated dead epithelial flakes may adhere to skin surface. E.g.
dandruff, psoriasis, dry skin.
Sakhawat Baloch 48
4. Crust: -
Dried residure of serum, blood or pus, on the skin surface. Large adherent crust is a scab e.g.
Impetigo, eczema.
5. Scar: -
Skin mark left after healing of wound.
6. Lichenification: -
Thickening and roughening of the skin e.g. contact dermatitis.
MYCOTIC (FUNGAL) INFECTION
The fungi, tiny representative of the plant kingdom that feed on the organic matter are
responsible for various skin infection. The fungal skin infections are:
1. Tenia Corporis (Body Ringworm): -
Tinia corporis affects the face, neck, trunk and extremities. It is also called ringworm because
ring shaped lesions appear. All the species of fungi may cause this disease but Tricophyton
Rubrum is the most common pathogen.
Its signs & symptoms are itching, lesions are ring of errythemia have scaly border and central
clearing.
Differential Diagnosis: -
 Secondary syphilis lesions are seen on palmer and planter mucus membrane.
 Psoriasis lesions mostly on elbow, knee, scalp and nail.
2. Tinea Cruris (Interinguinal): -

Marked itching in intertriginous areas, usually sparing the scrotum. Itching is severe. The
lesions have sharp margin and cleared center. Follicular pustules some time encountered.
Differential Diagnosis: -
In seborrhea dermatitis scrotum no lesion with margin.
3. Tinea Manum & Pedis ( Athlete foot): -
Tinea of the palm & foot, presenting with asymptomatic scaling. Fissuring in toe maceration in
toe web space.
Itching, burning and stinging of inter digital web
Prevention of Tinea Pedis: -
 The essential factor for prevention is personal hygiene.
 Careful drying between the toes after showering.
 Socks should be changed frequently.
 Apply dusting & drying powders as necessary.
 Proper use of anti fungal cream.
4. Tinea Capitis (Ringworm of scalp): -
It is fungal infection of hair shaft and common cause of hair loss. Clinically one or several
round, red, scally patches are present. As the hair in effected areas invaded by the fungi, they
becom brittle and break off at the surface of scalp, leaving bald patches.
Grisofulvin is an effective anti fugal agent. Topical creams are not effective.
Treatment
Sakhawat Baloch 49
Local Systematic
 Miconazole (Daktrain)
 Clitrionazole (Cenestin)
 Terbinafine (Terbisein) Grisofulvin Intracanazole
 Isocanazole (Isocan)(Travogen) 250-500 mg 200 mg daily
 Neftifine (Exoderil) twice daily for 2 weeks
IMPETIGO
It is contagious and autoinoculable infection of skin caused by staphylococci or streptococci.
Types: -
1. Vasoculopustula
2. Bullous type
1. Vasoculopustula: -
Thick golden crusted lesions caused by streptococci & staphylococci auerus.
2. Bullous type: -
Due to staphylococci aureus.

 Redness of skin due to congestion of capillary.
 vesicles, bullas, pustules, honey colored gummy crusts.
 When crusts are removed red areas are seen.
Treatment: -
Topical/Local Systematic
Mupirocin Neomycin Fusidic acid cephalexin Amosicillin &

(Bacterial Skin ointment (Fucidin) 500 mg B.D. Cloxicillin (Ampiclox)
ointment) Cream 500 mg T.D.S.
wet the lesions with pyodine.
Sakhawat Baloch 50
ATOPIC DERMATITIS (ECZEMA)
It is atopic, hereditary, and non-contagious skin disease characterized by chronic inflammation
of the skin. Major features include pruritis (itching) a typical morphology and distribution and
a personal or family history of atopy (asthma, hay fever, and atopic dermatitis)
Pathophysiology: -
It involves immunological abnormalities, such as elevated immunoglobulin E levels and
increased rates sensitization to common contact allergens and intradermal test. Almost 75%
of patient with this form eczema have a family history of atopic dermatitis, hay fever, or
asthma.
It is divided into three stages based on clinical appearance of the lesions.
1. Acute : Moderate to intense erythema, vesicles, a wet surface and severe itching.
2. Subacute: Erythema and scaling present in various patterns with indistinct borders.
Irritation, allergy, or infection can convert a subacute process into and acute one.
3. Chronic: The inflamed area thickens and the surface skin markings become more
prominent. Lichenification is the hallmark of chronic eczema. The surface of the skin is
dry and the border of the lesion well defined. There is moderate to intense itching.
1. Clinical diagnosis based on evaluation of the aggregate of signs, symptoms, course,
and associated familial findings.
2. Skin biopsy may be performed if clinical finding are in doubt.
Management: -
1. Topical:
A. Acute & weeping Lesions: -
 Use saline solution for washing.
 Use steroid in the form of cream instead of lotion.
B. Subcutaneous/Scaly lesion: -
The steroids are used in the form of ointment.
C. Chronic/Lichenification lesions: -
They are best treated with ointment.
Sakhawat Baloch 51
2. Systematic:
Cortisone (predisone 40-60 mg daily)
Nursing Care: -
 As atopic people are sensitive to low humidity and often get worse in winter.
 Simple soap should be used avoid wash cloth & brushes to the effected part.
 Avoid dry soap for bathing.
 After bathing skin should be patted dry (not rubbed).
 Immediate cover the effected site part with thin film of emollient such as Vaseline,
very hot bathes may increase itching so avoid from hot bathing.
 Advanton (methyl predisolon) cream & ointment.
 Dermovate (Clesbestasol) cream & ointment.
 Betnovate (Belimethasone) cream & ointment.
CONTACT DERMATITIS
Contact dermatitis is inflammation of the skin caused by exposure to external agents which
may affect various parts of the body.
Irritant contact dermatitis can occur in any person or contact with a sufficient
concentration of the irritant. Irritants include wool, glass, fibers, acid, alkaline, solvents,
detergents, oils found in clearing compounds, urine, feces, toxins from insects or aquatic plants
etc…
Allergic Contact dermatitis is cell-mediated hypersensitivity immune reaction from contact
with a specific antigen. Antigens include poison, ivy, synthetics, industrial chemicals, drugs
etc..
Clinical Manifestations: -
1. Itching, burning, erythema and vesiculation at point of contact.
2. Progression to weeping, crushing, drying, fissuring and peeling.
3. Lichenification (thickening of skin and pigmentation changes may occur with
chronicity.
Management: -
 Topical or oral steroids.
 Removal or avoidance of causative agents.
 Antipruritis systemic or topical antihistamines.
 Desensitization to poison or other substance
Nursing Consideration: -
1. Take through history to determine causative agents or contribution factors.
2. Teach patient to use allergen free products, wear gloves and protective clothing.
Wash and rinse skin thoroughly and wash clothing after contact.
Sakhawat Baloch 52
PSORIASIS
This is the hereditary non-infectious inflammatory disease of the skin in which abnormal
production of epidermal cells characterized by silvery scales mostly effects the elbow, fingers,
knee, abdomen, back etc. The production of epidermal cells occurs at a rate that is
approximately six to nine times faster than normal. The cells in the basal layer of the skin
divide too quickly and the newly formed cell move rapidly to the skin surface, that may
become evident as profuse scale of epidermal tissue.
Causes: -
The disease stems from a hereditary defect that causes over-production of keratin. But the
actual cause is still unknown.
 Red, raised plaques of skin covered with silvery scale.
 Plaques usually arises on the knees, elbow and scalp.
 If nails are involved, the nail findings are pitting with onycholysis.
 Mild itching
Diagnosis: -
Plaque like lesions mostly confirm the diagnosis.
Management: -
 Polytar (purified coaltar) liquid.
 Casoderm (Antipsoriatic/steroid) ointment.
 Daivonex/Dovonex (calcipetriol).
Nursing Care: -
 The nurse explains with sensitivity that currently there is no treatment of psoriasis
and life time management is essential to control the severity of disease.
 Educate the patient that minor injuries, cuts, stress, sun burn, infections can
exacerbate the disease.
 Advice the patient not to scratch or pick the effected area.
 Measures should be taken to prevent from skin dryness.
 Too frequent washing may cause soreness and scaling.
 Skin should be dried by patting, not by rubbing.
 Emollient should be applied for moisturizing.
 Instruct the patient not expose the area in sunlight.
BURN
Sakhawat Baloch 53
Transfer of energy causes burns from a heat source to a body. Heat may be transfer through
conduction or electromagnetic radiations. There are three main types of burn i.e. thermal,
radiation and chemical.
The depth of burn injury depends upon the temperature of the burner agent and the duration of
contact with agents.
Systematic response to Burn: -

The pathological changes resulting from major burn during the initial burn-shock period
include tissue hypo perfusion and organ hypo function secondary to decreased cardiac output.
Patients whose burn does not exceed 20% of their body surface, primary have localized effects.
The initial body response to a major burn injury homodynamic instability that results from the
shift fluid, sodium and protein from blood into interstitial spaces.
Cardiovascular Response: -
A fluid loss continues and vascular volume decrease, cardiac continues to fall and blood
pressure drop. This is the onset of burn shock. In response the sympathetic nervous system
release chatecholamine, it causes peripheral vasoconstriction, further decrease cardiac output.
Effects on fluid Electrolytes: -
Due to burn, the body fluid is decreased, sodium level is also reduced.
Degrees of Burn: -
1. Superficial (First Degree): -
In this only epidermis is involved. E.g. sun burn & low intensity flash.
2. Partial-Thickness (Secondary Degree): -
In this the epidermis & part of dermis is involved e.g. scald & flesh flame.
3. Full-Thickness (Third Degree): -
In this degree, the epidermis, entire dermis & sometimes subcutaneous tissue involves.
E.g. flame, prolonged exposure & hot electric current.
Sakhawat Baloch 54
Extent Of Body Surface Area Burned: -
Rule Of Nine: -
 Head & neck = 9%
 Each arm = 9%
 Anterior chest & abdomen = 18%
 Posterior = 18%
 Pubic area = 1%
 Each leg = 18%
Care Of Patient With Burn: -

1. Extinguish the flames: -
When clothes catch on fire, the flames can be extinguish if victim falls to the floor/ground.
2. Cool the burned area: -
In this step, the burnt area is soaked with cold water.
3. Remove restrictive objects: -
Although adherent clothing may be left in place, other clothing and all jewelry should be
removed.
4. Cover the wound: -
This prevents the bacterial infection. Decrease the pain by preventing air from coming into
contact.
5. In case of chemical burn irrigate wound immediately.
6. Assess the patient for shock.
7. Maintain the airway to enhance breathing.
8. Replacement of fluid.
9. Antibiotic therapy to prevent from secondary infection.
10. Maintain the I/O chart.
11.The local best drug sulfer sulfediazne e.g. Quinch Cream.
Management Of Burned Area: -

 Cleaning the area with N/Saline solution.
 It may be washed with pyodine solution.
 Sulfer sulfediazine cream i.e. Quinch is the drug of choice for local use.
 Inj. Ringerlactate solution
 Oral/Inj. Antibiotic (penicillin, cefhalosporin).
Sakhawat Baloch 55
HERPES SIMPLEX
It is a viral acute vesicular eruption caused by herpes simplex virus type 1 and 2. Type 1
caused cold sores or fever blisters – an eruption of blisters that often occurs during the course
of or after one of a variety of disease associated with fever (most commonly colds, influenza,
and pneumonia). The blisters usually appear around the mouth and on the lips (herpes
labialise); about the nose, face, and ears and in the mouth & pharynx.
The second type of herpes simplex virus is the usual cause of genital herpes {sexual
transmitted infection}.
Clinical Manifestaions: -
1. Prodormal pain, burning or tingling possible fever malaise.
2. Tiny vesicles appear on erythematous, swollen base; they rupture forming painful
ulcers, crushing, and eventually healing.
3. Can occur anywhere, especially the mucocutaneous junctions.
4. Vial shedding may occur between symptomatic period, leading to transmission of
infection.
Complications: -
1. Eczema Herpetium.
2. Herpetic whitlow (infection of the pulp of the fingertip with herpes type 1 & 2.
3. Neonatal infections occur during delivery by contact of infant with mother’s active
ulceration. Fetal anomalies include skin lesions, microcephaly, encephalitis.
1. Tranck smear
2. vial culture.
Management: -
1. Antiviral treatment with Acyclovir, famciclovir and valciclovir.
2. Analgesic
Nursing Care: -
1. Teach patient that it can transmitted by close and sexual contact, good hygiene and
hand washing are required, sexual abstinence or use of condom.
2. Recurrence may be brought by illness, emotional stress, pregnancy, sunlight and
other factors.
3. Advice patient with active herpes simples infection to avoid contact with
immunosupressed individuals because herpes simplex infection can be severe in these
individuals.
4. Tell patient that the lesions resolve in 1-2 weeks without scarring.
Sakhawat Baloch 56
SCABIES
Skin disease caused by a tiny parasite called an itch mite which burrows into the epidermis.
Scabies causes severe itching and is highly contagious. Itch mites are usually spread by close
skin-to-skin contact with an infected person. Sexual contact is an other means of transmission.
The itch mite that most commonly causes scabies is the female of the species Sarcoptes
scabiei.
Clinical Manifestaitons: -
It attacks about 4 weeks from time of contact for the patient’s symptoms to manifest
1. Itching, more intense at night.
2. Small erythematous papules and short, wavy burrow are seen on skin surfaces.
3. Frequently seen between fingers and groin area.
4. Spares head and scalp, except in children under 1 year of age.
Diagnostic Assessment: -
Parasite identifies by microscopic examination of skin scraping.
Management: -
1. Treated with anti-parasitic such as lindance, permethrin or crotamiton & Benzyl
benzonate.
2. Machine wash & dry clothing and linens on hot cycle.
3. Topical or systematic steroids may be needed to symptoms of allergic reactions of
scabies.
Nursing Considerations: -
1. Teach proper use of medication.
2. Advice patient to avoid close contact for 24 hours after treatment to prevent
transmission..
3. Tell the patient that itching may persist for days to weeks following treatment.
Sakhawat Baloch 57
ENDOCRINE SYSTEM
ASSESSMENT OF ENDOCRINE SYSTEM
Health History: -
 During the health history, patient asked for fatigue and changes in usual
fatigue and energy level.
 The patient is asked about in heat and cold tolerance.
 Recent changes in weight increased or decreased may occur in adrenal and
thyroid disorders.
 Changes in sexual functions and secondary sex characteristic may occur in
with any number if endocrine disorder.
 Changes in mood, memory and sleep.
Physical Assessment: -
Patient is observed for obvious changes in appearance that may indicate endocrine dysfunction for
example changes in skin are common with both hypo function and hyper function of thyroid gland.
Eye change may occur in with exopthamos of hyperthyroidism and graves disease. Changes in
physical appearance i.e. appearance of facial hair in women, moon face, buffalo hump, thinning of
skin, obesity of trunk and thinness of extremities, increased size of feet and hands, edema.
Vital sign are measured in physical assessment. Hypertension may occur with hyper function of
adrenal cortex or tumor of adrenal medulla. Hypotension may occur in hypo function of the adrenal
cortex. Tachycardia may be noticed.
Radioactive Iodine Therapy: -
The goal of the treatment with radioactive Iodine (123I or 131 I) is to destroy the over thyroid cells. Use
of radioactive iodine is most common treatment in elderly patients. Almost all the iodine that enters
and is retained in the body becomes concentrated in thyroid gland. Radioactive isotope of iodine is
concentrated in thyroid gland, where it destroys thyroid cells. In radioactive therapy a single oral dose
of agent (Radioactive iodine 123 I or 131 I) is administered by the radiologist.
Dose is based on 80-160 uG/g estimated thyroid weight. About 70% to 85% of the patients are cured
by one dose of radioactive iodine.
An additional 10% to 20% require two doses, rarely third dose necessary.
Radioactive has been used in toxic adenomas and multinodular goiter and thyrotoxicosis. A major
advantage of use of radioactive iodine is that it avoids may of side effects.
Sakhawat Baloch 58
ADDISONS DISEASE
Addisons disease is caused by a deficiency of cortical hormones. OR Adrenocortical
insufficiency is known as Addisons disease.
Causes:
 Adrenal cortex is surgically removed with bilateral adrenalectomy.
 Infections such as tuberculosis and histoplasmosis.
 Inadequate secretion of ACTH from pituitary gland.
 Muscular weakness
 Anorexia
 Gastrointestinal symptoms
 Fatigue
 Dark pigmentation of the skin
 Hypotension.
 Low blood glucose
 Low serum sodium
 High serum potassium
 Restlessness
Investigations: -
 Serum electrolytes: In serum increased concentration of serum potassium
and decreased concentration of sodium and decreased the concentration of
blood glucose.
 Blood CP: Increased white blood count Leucocytosis.
Management: -
 Restore blood circulation.

 Hydrocortisone (Solu-Cortef) is given I/V and followed with 5% Dextrose saline.
 Monitoring vital signs
 Administer of fluid
 Check vital signs and maintain I/O chart daily.
 Fluid balance measure should be taken
 Weight change record daily.
 Patient skin turgor is assessed.
 Oral intake may be initiated as soon as tolerated by patient, intravenous fluids are
decreased as oral fluids are accepted.
 Improved activity in tolerance.
 Reassure the patient to relieve anxiety or confusion.
Sakhawat Baloch 59
CUSHING’S SYNDROME
Hypersecretion of cortical hormones from adrenal cortex from adrenal gland. It is opposite of
the addisons disease.
Causes: -
 Excessive administration of cortisone.
 Hyperlapsia of adrenal gland.
Pathophysiology: -
The basic lesions responsible for Cushing’s syndrome may be the tumor of the pituitary gland
that produces ACTH and stimulates the adrenal cortex to increase the hormones secretion
despite the adequate amount being produced. Primary hyperlapsia of adrenal gland of pituitary
gland is less common.
Administration of cortisone or ACTH may produce Cushing’s syndrome.
 Obesity with a fatty “buffalo hump”
 Skin is thinned, fragile and easily traumatized.
 Weakness
 Sleep disturbance.
 Lassitude
 Muscle wasting
 Osteoporosis.
 Kyphosis.
 Hypertension
 Moon like face
 Increased oiliness skin and acne.
 Weight gain
 Hyperglycemia
 Hirsectism (excessive hair growth on face)
 Mood changes, distress, depression.
Investigations: -
 Serum electrolytes
 Blood CP
 Radio immunoassay of plasma ACTH
 CRF (coticotropic Releasing Factor stimulating test).
 CT scan
 MRI
Management: -
 Transphenoid hypophysectomy (surgical removal of tumor of pituitary galnd.
(Pituitary ademosis)
Sakhawat Baloch 60
 Adrenolectomy: Adrenolectomy is indicated for adrenal tumor or
hyperplasia.
 If patient is not cope surgery then patient treated with mitotine (Lysoeren)
that drug suppress cortisol production.
 Reassure the patient
 Check vitals.
 Provide diet low in sodium
 Monitor daily weight, intake and output, and laboratory values of sodium,
potassium and choride.
 Decrease controllable stressors (explain all the procedures stowhy and
carefully.
 Provide neat and clean bed
.
DIABETES INCIPIDUS
Diabetes incipidus a disorder of posterior lobe of the pituitary gland due to deficiency of vasopression.
The antidiuretic hormone.
Etiology: -
The cause of pituitary D.I. may be central brain or pituitary tumors, head trauma, encephalitis,
meningitis, hypophactomy or cranial surgery, chronic renal failure, sickle cell anemia.
Pathophysiology: -
The lack of adequate ADH or an ineffective kidney response to ADH results in insufficient water re-
absorption by kidney. The loss of excessive water from body (polyuria) stimulates the perception of
thirst.
 Polyuria.
 Polydipsia
 Hypertension
 Tachycardia
 Poor skin turger
 Mental dullness
 Weight loss
Management: -
 The therapeutic goal is maintained of fluid and electrolytes balance.

 I/V administration of fluid (saline and glucose).
Sakhawat Baloch 61
 Carbamazepine (Tegretol)
 Hormone replacement with ADH (vasopression) administer either SC, I/M
i.e. Arginine Vavopression 0.25-0.5 mg SC or I/M.
 Maintain fluid and electrolyte balance.
 Monitor intake and output daily.
 Check vitals and weight daily.
 Administered as per order.
 If hypertension restrict sodium in diet
ACROMEGALY
Hypersecretion of growth hormone from anterior lobe of the pituitary gland.
Causes: -
Macro adenoma within the pituitary gland.
 Increase in size of nose, lips, prominent of supra orbital ridges, increased
growth of mandible, facial puffines.
 Enlarged tongue, increase size of hands, nose, cardiomegaly, spleenomegaly.
 Increased blood pressure.
 ACNE, Bachache, arthritis.
 Peripheral nerve damage.
Investigations: -
 MRI
 CT scan.
Management (surgical): -
 Pituitary adenomas are treated with surgery, radiation.
 Drugs suppress the hypersecretion of adenoma.
Medical Management: -
 Bromocriptine
 Dopamine agonist
 Reassure the patient
 Check vital signs (TPR & BP)
 Teach about body image.
 Relieve anxiety.
Sakhawat Baloch 62
 Assistance needed with activities of daily living.
PITUITARY DWARFISM
Pituitary dwarfism is a condition of growth retardation in which the patient are very short but have
normal body proportions. Some children have this condition go through delayed but normal puberty
and have normal reproductive capabilities and other have never become sexually mature.
This is caused due to deficiency of growth hormone
Sign and Symptoms: -

 Slow growth or absent increase in weight.
 Absent or delayed sexual development.
 Headache.
 Excessive thirst.
Investigations:
 C.T scan
 MRI
GIGANTISM
It is caused due to excessive growth in height is due to excessive production of growth hormone
acedophill cell hyperplasia or from acidophill aadenoma of the anterior lobe of pituitary gland.
Causes: -
 Hyperplasia , Acedophill adenoma.
 It is usually found in men.
 Height between 7 to 8 feet.
 Enlargement of the feet and hands.
 Enlargement of the mandible.
 Muscle weakness
 Hypertension.
Diagnostic Criteria: -
 C.T. scan ,MRI
Treatment: -
 Bromocriptine 2.5 mg TDS.
Bromocripton causes nausea & vomiting
THYROIDECTOMY
Partial or complete thyroidectomy may be carried out as primary treatment of the thyroid carcinoma,
hyperthyroidism or hyperparathyroidism. The type of surgery and extent of surgery depend on
diagnosis, goal of surgery and prognosis.
Sakhawat Baloch 63
Pre-operative Management: -
1. Pharmacotherapy: -
Before undergoing surgery for treatment of hyperthyroidism, the patient is treated with
appropriate medication to return the thyroid hormone level and metabolic rate to normal and to
reduce the risk of thyroid storm and hemorrhage during post-operative period.
Stop prolong cotting medications i.e. asprin before several weeks to surgery to
minimize the risk of post-operative bleeding.
2. Reduce Anxiety: -
One important approach in pre-operative period is to gain the confidence of the patient and
reduce anxiety.
3. Supplement of vitamins particularly thiamine and ascorbid acid are provided.
4. Tea, coffee, cola, and other stimulant are avoided.
Pre-operative Preparation: -
 Take vital signs
 All necessary diagnostic tests performed before surgery.
 Special efforts are made to ensure a good night rest preceding surgery.
 Take the consent from the patient or their relatives.
 Give O.T. dress.
 Patient education: Pre-operative teaching includes demonstrating to the patient how to
support the neck with hands after surgery to prevent stress on the incision.
Post-operative Management: -
 Patient is moved and turned carefully to support the head and avoid tension on
sutures.
 Provide most comfortable position, semi-fowlers position with head elevated and
supported by pillows.
 Analgesic are administered as prescribed for pain.
 I/V fluid are administered during the immediate post-operative period.
 Initially cold fluid and ice may be taken better than other fluids.
 Advice soft diet.
 Surgical dressing are assessed periodically.
 Anterior dressing must be observed for bleeding.
 Advice the patient to talk as little as possible.
 As patient usually is permitted out of bed as soon as possible and encouraged to
eat food that are easily eaten. A well-balanced high calories diet is prescribed to
promote weight gain.
Pharyngitis
It is an infection or inflammation of throat. Usually 70% caused by viral organism. And also
streptococci can cause acute Pharyngitis. It is characterized by sore throat with pain and fever.
Sakhawat Baloch 64
 Red pharyngeal membrane and tonsils
 Fever
 Pain
 Sore throat
 Hoarseness
 Malaise
Investigations: -
 Blood CP
 Blood Culture
 Throat Culture
Medical Management: -
Viral Pharyngitis is treated with supportive measures since antibiotics will have no effect on
viral organism.
 Antibiotic may be used to bacterial Pharyngitis.
 Penicillin is also used.
 Erythromycin is also used.
 Antibiotic are used at least 10 days.
 If there is difficulty id swallowing, advice I/V fluid.
 If patient cannot swallow, then advice soft diet.
 Analgesic should be given.
 Antitussive medication should be given i.e. (codeine, dextromethorph or
hydrocodone are given for painful cough.
 Encourage bed rest.
 Reassure the patient.
 Take vital signs.
 Secure nasal swabbing and throat and blood specimens for culture as need.
 Administer warm saline gargles to ease pain.
 Perform mouth care to prevent the fissures of lips and inflammations of mouth.
TONSILITIS
The tonsils are composed of lymphatic tissue and are situated on each side of oropharynx. This is the
inflammation of tonsils. Most commonly, it is caused by streptococci. It may be caused by:
 Bacteria – streptococci and staphylococci.
 Virus – influenza virus
 Allergy
Sakhawat Baloch 65
 Sore throat
 Fever
 Difficulty in swallowing
 On inspection, inflammation of tonsils
 Hyperemia of tonsils
 Enlargement of tonsils
 Pus spots on tonsils
Treatment: -
 Syp. Penicillin 250 mg orally T.D.S. or 500 mg OD for 10 days.
 Cefuroxine (Zennat Syp: Tab. 250 mg.
 Ampicillin + Cloxicillin (Ampiclox) 500 mg 6 hourly.
 Azithromycin (500 mg once daily) for 3 days.
 Anti-Allergy medication.
 Tab. Ponstan.
Post operative care of patient after tonsillectomy: -

1. In immediate post operative period, the most comfortable position is prone position
with head turned to side to allow for drainage from mouth and pharynx.
2. the oral airway is not removed until patient swallowing reflex has returned.
3. An ice collar is applied to the neck.
4. Hemorrhage is potential complication after tonsillectomy.
5. Assess the vitals i.e. BP, temp. Pulse etc.
6. Assess for the complications.
7. Tonsillectomy generally doesn’t require more hospitalization and are performed as out
patient surgery with a short length of stay, usually hemorrhage occurs in first 12-24
hours.
8. Alkaline mouthwashes and warm saline solution are useful in coping with the thick
mucus that may be present after a tonsillectomy.
9. A liquid or semi liquid diet is given for several days.
10. Milk and milk products (ice cream) may be restricted because they tend to increase
mucus increased.
Sakhawat Baloch 66
LARYNGITIS
This is an inflammation of larynx.

Causes: -
1. Voice abuse
2. Smoking
3. Exposure to dust
4. Pollutant
5. Season (Winter)
6. Pathogen
a) Bacteria
b) Virus
c) Allergy
Signs & Symptoms: -
 Hoarseness
 Resting voice
 Cough
 Loss voice
 Fever
Management: -
 Antibiotic
 Anti-allergic
 Anti-inflammatory
 Resting the voice
 Eliminating the respiratory tract infection.
 Excessive use of voice should be avoided.
 Avoid smoking
 Increase humidity in home or room/ward.
 Avoid fried and fatty dishes.
Complications: -
 Pharyngitis
 Gingivitis
 Otitis
 Mouth ulcer
 Bronchitis
 Trachitis
Sakhawat Baloch 67
Sakhawat Baloch 68

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Medical surgical Nursing-III

UNIT NO: 1: NEUROLOGICAL NURSING

A) Examination of mental status: -

B) Language & Speech:-

The Common diagnostic studies are:

1. Cerebro spinal fluid analysis :-

3. Magnetic Resonance Image (MRI): -

Class V: Intubations needed to maintain airway

Sign & symptoms:-

This refers to a peripheral facial paralysis characterized by a disruption of motor branch of

Trauma: Physical trauma,

Acute and chronic otitis media

Sign & symptoms: -

Post Operative Care: -

D. During the headache at least one of the following:

This is an inflammation of the polyneurons characterized by varying degree of motor weakness or

Physiology Of Musculo-Skeletal System

9. Patient education at Home for Cast Management:

Managing The Patient In Traction

 Assess the patients neurovascular status.

A. Factors Enhancing Fracture Healing:

B. Factors Inhibiting Fracture Healing:

Time Necessary For Union Of Bones:

Osteomyelitis is an infection of bone by direct or indirect invasion of an organism. Bone infection is

 Pagetic bone has a characteristic appearance on x-rays. A skeletal survey is

In general, patients with Paget's disease should receive 1000-1500 mg of calcium,

Usually no treatment is recommended for the patient without symptoms.

Rheumatoid arthritis is a chronic inflammatory disease characterized by recurrent

Causes & pathophysiology: -

It can be explained by four stages.

Signs & Symptoms: -

High fever Heat Hot flushes

Aging Acne Coritsone deficiency

MYCOTIC (FUNGAL) INFECTION

2. Tinea Cruris (Interinguinal): -

It is contagious and autoinoculable infection of skin caused by staphylococci or streptococci.

Signs and Symptoms: -

Mupirocin Neomycin Fusidic acid cephalexin Amosicillin &

wet the lesions with pyodine.

Systematic response to Burn: -

Care Of Patient With Burn: -

Management Of Burned Area: -

ASSESSMENT OF ENDOCRINE SYSTEM

 Restore blood circulation.

 The therapeutic goal is maintained of fluid and electrolytes balance.

Sign and Symptoms: -

Post operative care of patient after tonsillectomy: -

This is an inflammation of larynx.

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