DELTA University

Faculty of Nursing
Critical Care and Emergency Nursing Department

CRITICAL CARE AND EMERGENCY

BOOK

Prepared By

Critical Care and Emergency Nursing Department

Second year, the 2nd semster

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 Chest Injuries

At the end of the lecture, the student will be able to:

1. Enumerate types of chest injury.
2. List Complications of Chest Injuries
3. Discuss the eventual disposition of chest trauma patients based on their
diagnosis.
4. Appreciate the necessity for emergent intervention in certain chest trauma
conditions
Types Chest Injuries:
It classified into closed & open chest injuries.
Closed Chest Injuries
- The skin is not broken
- Blunt trauma
Open Chest Injuries
- Chest wall itself is penetrated by some object as knife, piece of metal or broken
end of fractured rib.
Complications of Chest Injuries
1. Pneumothorax
2. Hemothorax
3. Flail Chest

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 Pneumothorax

 Accumulation of air in the pleural space

 Called collapsed lung
 Air enters through a hole in the chest wall or the surface of the lung as the
patient attempts to breath, causing the lung on that side to collapse
 As result, any blood that passes through the collapsed portion of the lung is
not oxygenated, and hypoxia can develop.
 Depending on the size of the hole and the rate at which air fills the cavity,
the lung may collapse in a few seconds or a few hours.
Causes:
- Chest injury. Any blunt or penetrating injury to chest can cause lung collapse.
as physical assaults or car crashes,
- Lung disease. Damaged lung tissue is more likely to collapse. Lung damage
can be caused by many types of underlying diseases, such as chronic
obstructive pulmonary disease (COPD), cystic fibrosis, lung cancer or
pneumonia. Cystic lung diseases that cause round, thin-walled air sacs in the
lung tissue that can rupture, resulting in pneumothorax.
- Ruptured air blisters. Small air blisters (blebs) can develop on the top of the
lungs. These air blisters sometimes burst — allowing air to leak into the space
that surrounds the lungs.
- Mechanical ventilation. A severe type of pneumothorax can occur in patient
who needs mechanical assistance. The ventilator can create an imbalance of air
pressure within the chest. The lung may collapse completely.
Types of Pneumothorax
1. Spontaneous pneumothorax:
- occurs without an obvious etiology such as trauma or iatrogenic
causes. can be classified as either primary or secondary.
Primary spontaneous pneumothorax (PSP):

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- Occurs when the patient does not have a history of the underlying
pulmonary such as lung disease or rib fracture.
- Primary spontaneous pneumothorax is likely due to the formation of small
sacs of air (blebs) in lung tissue that rupture.
- Many things can cause a bleb to rupture, such as changes in air pressure or
a very sudden deep breath.
Secondary spontaneous pneumothorax (SSP):
Is associated with a history of an underlying pulmonary disease.
2. Tension pneumothorax:
- Can develop from any type of pneumothorax such as traumatic chest injury
as a stab wound or a gunshot; or a closed trauma, like a rib fracture or in
patients breathing through mechanical ventilation.
Signs and symptoms of tension pneumothorax

2. Severe shortness of breath, shallow breathing

3. acute chest pain, along with low blood oxygen levels
4. Increased heart rate, low blood pressure, and altered mental status.
5. tracheal deviation away from the affected side
6. Decreased or absent breath sounds upon lung auscultation
7. Hyper resonant chest percussion, and asymmetrical expansion of the chest
due to the collapsed affected lung.
8. In severe cases, individuals can present blue discoloration of the skin due
to decreased oxygen levels in the blood, and distended neck veins as a
result of the collapsed blood vessels that should return blood to the heart.
9. Sometimes, the air in the pleural space can leak and be trapped in nearby
areas, such as the subcutaneous tissue, which is known as subcutaneous
emphysema, as well as nearby cavities like the mediastinum, causing a
pneumomediastinum.

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Treatment of tension pneumothorax
 Requires immediate decompression of the trapped air by placing a 14- or
16-gauge needle into the pleural space, usually between the second to
fourth anterior intercostal spaces.
 An immediate rush of air should escape and the patient’s ventilation
should improve.
 Supplemental oxygen is provided to the patient before decompression.
 After emergent decompression, the needles are changed to chest tubes.
This is done to allow the lungs to expand as well as to prevent a
reoccurrence.
 a chest X-ray can be performed to check the location of the tube
 Last, additional assessment is necessary to determine the cause of tension
pneumothorax. The nurse must continue to assess and reassess the
patient.

Hemothorax
- Hemothorax is a collection of blood in the space between the visceral and
parietal pleura (pleural space).
- The most common mechanism of trauma is a blunt or penetrating injury to
intrathoracic or extrathoracic structures that result in bleeding into the
thorax.
- Bleeding may arise from the chest wall, intercostal or internal mammary
arteries, great vessels, mediastinum, myocardium, lung parenchyma,
diaphragm, or abdomen.
Signs and symptoms include:
- rapid breathing, restlessness, shock, and pale, cool, clammy skin
- When the affected area is percussed, a dull feeling may be observed.
- Neck veins may be flat and breathing sounds reduced.

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- It can also cause a collapsed lung (atelectasis).
- Massive hemothorax, often defined as over 1.5 liters of blood initially
when an intercostal drain is placed, or a bleeding rate greater than .2
liters/hr, can result in shock with two causes: massive bleeding resulting
from hypovolemic shock, and venous pressure from the retained blood,
impairing blood flow.
Treatment of Hemothorax:
 Chest tube insertion with chest tube drainage system
 Blood transfusions: If there is significant blood loss,
 a blood transfusion may be necessary to replace lost blood volume.
 Treatment of hypovolemia as necessary
Flail Chest
- Ribs may be fractured in more than one place.
- If 2 or more ribs are fractured in 2 or more places or
- If the sternum is fractured along with several ribs
- Also called Paradoxical motion (chest wall moves opposite of normal
instead of out during inhalation, out instead of in during exhalation)
- Breathing is painful and ineffective
- Flail segment interferes with the body’s normal mechanics of ventilation
- Hypoxia
Treatment of Flail Chest
 Stabilize flail rib segment with tape a bulky pad against that segment
and taping too tightly
 Immobilization of flail segment with tape a bulky pad against that
segment and taping too tightly will also decrease pain and provide
adequate ventilation, see the following figure.

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  Cover sucking chest wound with nonporous dressing taped on three
sides
 Maintain airway
 Providing respiratory support if needed
 Give O2
 Ongoing assessment for possible Pneumothorax
 Positive pressure ventilation
 Chest tube insertion with chest tube drainage system

Traumatic brain injury

Introduction:
- Traumatic Brain Injury (TBI) may result from anywhere between simple
blows to the head to a penetrating injury to the brain. The frontal and
temporal areas of the brain are the main areas involved.
The mechanisms of traumatic brain injury

- Traumatic brain injury occurs when physical or external forces impact the
brain either from a penetrating object or a bump, blow, or jolt to the head.
- Open traumatic brain injury occurs when the skull is pierced by an object
by a bullet, shrapnel, and bone fragment or by a weapon such as a hammer,
knife, or baseball bat.
- Closed traumatic brain injury or blunt traumatic brain injury caused by
an external force that produces movement of the brain within the skull such
as falls, motor vehicle crashes, sports injuries, or being struck by an object.
Classification of traumatic brain injury
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 1- Direct (primary brain injury)
• Primary injury caused by forces of trauma
2- Indirect (secondary brain injury)
• Secondary injury caused by factors resulting from the primary injury
1- Primary Brain Injury:
- Primary injury is the result of the initial injury. This may include
contusions, lacerations.
- The initial injury causes disruption of the electrical, chemical, and physical
integrity of the cells in the area, leading to cell death.

The following are the different types of brain injury:

1. Concussion:
- This is usually a mild TBI without any gross structural damage and occurs
secondary to a non-penetrating TBI.
- It usually results from acceleration/deceleration forces occurring secondary
to a direct blow to the head.
- It causes a transient altered mental status, which can range from confusion
to loss of consciousness.
2. Extra-axial Hematoma:
- Extra-axial hematomas include both epidural hematomas (EDH) and
subdural hematomas (SDH).
- -EDH usually results from bleeding from the middle meningeal artery and
its branches or a fracture and is usually acute.
- -SDH can result from the bleeding of a bridging vein and can be acute or
chronic.
3. Contusion:
- Contusions (bruising of the brain) can be a coup or contrecoup type.

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- Coup contusions occur at the site of impact,
- Contrecoup injuries typically take place on the contralateral side of impact,
usually the basi-frontal lobe and anterior temporal lobe.
4. Traumatic Subarachnoid Hemorrhage (SAH)
- is most commonly caused by trauma and results from the tearing of small
capillaries with blood subsequently entering into the subarachnoid space. It
commonly occurs over the convexity, whereas SAH secondary to
aneurysmal rupture occurs in the basal cisterns.

5. Diffuse Axonal Injury (DAI)

- This can underlie mild to moderate TBI and potentially results from any
shearing, stretching, or twisting injuries to the neuronal axons.
B- Secondary traumatic brain injury
- Secondary brain injury encompasses all events leading to further brain
damage that occurs after the initiating trauma.
- Many conditions causing secondary brain injury are uncontrolled increased
intracranial pressure, cerebral ischemia, systemic hypotension and local or
systemic infection.
Classification of of traumatic brain injury by severity
1-Mild head injury:
- Determined by Glasgow Coma Scale (GSC) score of 13 to 15 with brief
loss of consciousness for a few seconds or minutes, post -traumatic amnesia
less than 1 hour of the TBI.
2-Moderate TBI:
- Results in loss of consciousness for 1 to 24 hours, with Glasgow Coma
Scale (GSC) score of 9 to12, with normal or abnormal brain imaging
results, post-traumatic amnesia from 1to7 days after the insult .
3-Severe TBI:
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 - Described as a loss of consciousness or coma for more than 7days with
Glasgow Coma Scale (GSC) score of 3to 8, abnormal brain imaging results,
post-traumatic amnesia more than 7 days.
Diagnosis of traumatic brain injury:
- Clinical history/presentation with thorough neurological (Glasgow
Coma Scale score)
- Labs: Serum levels of two biomarkers: Glial fibrillary acidic protein
(GFAP) and Ubiquitin C-terminal hydrolase (UCH-L1) correlated with the
degree of brain injury, with GFAP being the more reliable of the two up to
7 days after impact. They are proteins that leak from astrocytes and neurons
when are damaged.
- Neuroimaging:
 CT head and MRI are used to measure changes in anatomical or
physiological parameters of TBI.
 Diffusion tensor imaging (DTI) is used to detect axonal injury for mild
to moderate TBI.
 Functional MRI (fMRI) is often used to differentiate TBI from control
groups and has been used to study activation patterns in patients with
TBI.
 Brain Perfusion Single Photon Emission Computed Tomography
(SPECT) is used to measure cerebral blood flow and activity patterns.
It is indicated for the evaluation of TBI in the absence of anatomical
findings.
Medical management of traumatic brain injury:-
A- If no hemorrhage is present on CT or the patient meets criteria that do
not indicate CT is necessary:
1. If the patient has a GCS of 15 and no focal neurologic deficits, the patient has a
mild TBI and may be safely discharged.
2. If the patient had GCS of less than 15 or has any concerning exam findings, the
patient may require further evaluation. The patient may require further

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 laboratory studies or imaging. CT angiography or MRI merit consideration
if a non-contrast CT is non-diagnostic
B- If hemorrhage is present on CT:
1-Maintain adequate ventilation and oxygenation
- Maintain SpO2 of at least 92%
- In patients with GCS under 8, intubation should merit strong consideration,
as it is unlikely that they will be able to maintain their airway.
Intubation:
- Patients should be pre-oxygenated as the risk of hypoxia outweighs the risk
of hyperoxia. Historically lidocaine has been used for pre-treatment to blunt
sympathetic response to airway manipulation during laryngoscopy, but
studies have shown no definitive benefit.
- Propofol may be useful in lowering blood pressure, and thus the
intracranial pressure in hypertensive patients. It may also have anti-
epileptic effects.
- Paralytic agents such as rocuronium, vecuronium, or succinylcholine may
be kept in a consideration, however, these agents will limit the ability to
perform a neurologic exam after administration.
2- Maintain adequate circulation:
- Maintain normotension with target SBP greater than 90 and less than 140
- Initiate fluid resuscitation with normal saline with the goal of euvolemia.
- If the patient has hypotension that is refractory to fluid resuscitation,
vasopressor support should be initiated.
- Phenylephrine may be the best choice for a neurogenic shock as it has pure
vasoconstriction effects, and studies have shown that it increases cerebral
perfusion pressure (CPP) without increasing intracranial pressure (ICP).
- In patients who are bradycardia due to Cushing's reflex, norepinephrine may
be a better choice.
- Packed red blood cells should be transfused for a goal of Hb over 10 mg/dL in
severe TBI.
- Coagulopathy should be corrected.

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3- Maintain adequate cerebral perfusion and reduce intracranial pressure:
- Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) -
intracranial pressure (ICP)
- Elevation of the head of the bed to 30 degrees or reverse Trendelenburg
positioning can lower ICP
- Hyperosmolar therapy via Manitol using a bolus of 1 g/kg and/or hypertonic
saline (dosing depends on the concentration available and vascular access)
may be given to reduce ICP.
- Therapeutic cooling and medically induced comatose state are some measures
to reduce intracranial pressure. Some patients will need monitoring of the
intracranial pressure.
- Hyperventilation is somewhat controversial. It may be transiently helpful in
patients with increased intracranial pressure as hypocapnia may induce
cerebral vasoconstriction and transiently decrease the expansion of
hemorrhage; however, this is a temporizing measure to definitive
management.
- Prolonged hypocapnia may cause cerebral ischemia. Targeting low-normal
pCO2 of approximately 35 is reasonable
4-Seizures control:
- Patients with severe TBI, including GCS less than 10, cortical contusion,
depressed skull fractures, subdural, epidural, subarachnoid, or intracerebral
hemorrhage, penetrating head injury are at risk for seizures.
- Seizure activity that is apparent clinically or on EEG should receive
management with benzodiazepines and anti-epileptic drugs (AEDs).
- Propofol may be optimal for post-intubation sedation.
- AED prophylaxis should also is a viable option in severe TBI patients.
Phenytoin or fosphenytoin are first-line, levetiracetam is an alternative that
may have fewer side effects. Prophylaxis should last for 7 days.
2- Neurosurgery consultation:
- Is necessary for patients with intracranial hemorrhage. While some patients
may be monitored clinically and have repeat imaging studies to visualize if
there is expansion, definitive management may be required.

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 - A Burr hole may be an option to evacuate a hematoma in an emergent
setting with herniation.
- Patients may require a decompressive craniectomy. Patients may require
close monitoring of intracranial pressure via an extraventricular drain
Complications:
 Post-traumatic seizures
 Deep vein thrombosis Mood and behavior changes
 Hydrocephalus Spasticity

Spinal cord injury (SCI)

The intended learning outcomes:
By the end of this lecture every candidate will be able to:
- Predict mechanisms of injury that are likely to cause spinal injury.
- Distinguish between types of spinal injury.
- Describe prehospital evaluation and assessment of spinal cord injury.
- Distinguish between spinal shock, neurogenic shock, and autonomic
hyperreflexia syndrome.
Spinal cord injury (SCI)
- Is a serious medical condition. It occurs when the axons of nerves running
through the spinal cord are disrupted, leading to loss of motor and sensory
function below the level of injury.

Etiology:

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- The leading cause of spinal cord injury is motor vehicle collisions, falls,
violence, sports injuries, and from medical and surgical etiologies
Type of spinal cord injury:
1-Complete Transection of the Spinal Cor:
- These injuries typically demonstrate complete bilateral loss of motor
function, pain sensation, temperature sensation, vibratory sensation, and
tactile sensation below the level of injury.
2-Central Cord Syndrome:
- This is the most common incomplete SCI.
- Injury is caused by hyperextension of the neck leading to compression of
the cervical spinal cord, causing damage primarily to the center of the cord.
3-Anterior Cord Syndrome:
- Classically due to compromise of blood flow from the
anterior spinal artery.
- Bilateral injury to the spinothalamic tracts leads to bilateral loss of pain and
temperature sensation below the level of injury.
- Bilateral injury to corticospinal tracts leads to weakness or paralysis below
the level of injury.
4-Posterior Cord Syndrome:
- This injury pattern rarely occurs due to trauma. More often, injury is due to
infectious, toxic, or metabolic causes.
- Damage to dorsal columns causes loss of tactile sensation, proprioception,
and vibratory sensation.
5-Brown-Séquard Syndrome :
- Injury results from right or left-sided hemisection of the spinal cord.
6-Conus medullaris Syndrome:
- It is caused by injury to the terminal aspect of the spinal cord, just proximal
to the cauda equina. It occurs near lumbar vertebral levels 1 (L1) and 2
(L2),

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Functional Loss from Spinal Cord Injury (Based on Complete Lesions)
C1–C4:
- Tetraplegia: Loss of all motor function from the neck down
- Loss of involuntary (phrenic) and voluntary (intercostal) respiratory
function; Ventilatory support and a tracheostomy needed
- C5: Tetraplegia: Loss of all function below the upper shoulders
- C6 :Tetraplegia: Loss of all function below the shoulders and upper arms;
lacks elbow, forearm, and hand control
- C7: Tetraplegia: Loss of motor control to portions of the arms and hands
- Intact: Voluntary strength in shoulder depressors, shoulder abductors,
internal rotators, and radial wrist extensors
- C8:Tetraplegia: Loss of motor control to portions of the arms and hands
- Intact: Some voluntary control of elbow extensors, wrist, finger extension,
and finger flexors.
- T1–T6: Paraplegia: Loss of everything below the mid-chest region,
including the trunk muscles
- T6–T12:Paraplegia: Loss of motor control below the waist
- Intact: Shoulders, arms, hands, and long trunk muscles
- Loss of everything below the waist
- L1–L3:Paraplegia: Loss of L2–L4 (knee most control of jerk) legs and
pelvis
- Intact: Shoulders, arms, hands, torso, hip rotation and flexion, and some leg
flexion
- L3–L4:Paraplegia: Loss of control of portions of lower legs, ankles, and
feet
- L4 to S5:Paraplegia: Incomplete Segmental motor control
- L4 to S1: Abduction and internal rotation of hip, ankle dorsiflexion, and
foot inversion
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 - L5 to S1: Foot eversion
- L4 to S2: Knee flexion
- S1–S2: Plantar flexion (ankle jerk)
- S2–S5: Bowel/bladder control
- L5: Medial aspect of foot
- S1: Lateral aspect of foot
- S2: Posterior aspect of calf/thigh
- Sacral sensory nerves innervate the lower legs, feet, and perineum
- S2–S4 segments control urinary continence
- S3–S5 segments control bowel continence (perianal muscles)
Complication of spinal cord injury:
Autonomic Nervous System Dysfunction:
a) Spinal Shock
- Spinal shock is a condition that occurs immediately or within several hours
of an SCI;
- It is caused by the sudden cessation of impulses from the higher brain
centers. Because of a decrease in sympathetic innervation to the vascular
system, massive vasodilation occurs, which initiates decreases in preload
and stroke volume leads to a decrease in heart rate.
- The vasodilation also leads to a decrease in afterload, hypotension and
bradycardia.
Clinical Manifestations of Spinal Shock
- Flaccid paralysis below the level of injury
- Absence of cutaneous and proprioceptive sensation
- Hypotension and bradycardia
- Absence of reflex activity below the level of injury; may cause urinary
retention, bowel paralysis, and ileus

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 - Loss of temperature control (Vasodilation and inability to shiver make it
difficult for the patient to conserve heat in a cool environment, and the
inability to perspire prevents normal cooling in a hot environment.)
b) Neurogenic Shock:
- A form of distributive shock, is a condition seen in patients with severe
cervical and upper thoracic injuries.
- Signs and symptoms include hypotension, severe bradycardia, and loss of
the ability to sweat below the level of injury.
c) Autonomic Dysreflexia:
- Is a dangerous syndrome involving an overreaction of autonomic nervous
system, occurs in patient with SCI at or above thoracic spinal level 6 (T6).
- It causes a sudden and severe rise in blood pressure, bradycardia,
hypertension, facial flushing, and headache
- This condition is caused by a massive sympathetic response to noxious
stimuli (e.g., full bladder, line insertions, fecal impaction)
- Immediate intervention is needed to prevent cerebral hemorrhage,
seizures, and acute pulmonary edema.
d) Orthostatic Hypotension:
- Orthostatic hypotension may occur in a patient with an SCI because the
patient is unable to compensate for changes in position.
- The vasoconstriction message from the medulla cannot reach the blood
vessels because of the cord injury.
- Diagnosis of SCI
- -Computerized tomography (CT or CAT scan)
- -Magnetic resonance imaging (MRI) is needed to accurately assess the level
of injury to the spinal cord itself.
Emergency Assessment and Management

Pre-hospital Management:
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 - Immobilization can help prevent the worsening of any existing injuries.
- A primary survey performed at the scene of an accident includes a rapid
assessment of airway, breathing, and circulation (ABCs).
- Airway patency is assessed, and the cervical spine is immobilized and
stabilized.
- Cervical collar increases the level of stability but does not provide complete
stabilization
- Use of log-rolling maneuvers during movement of patients
Pharmacological treatment:
- High-dose methylprednisolone (Solu-Medrol) in the emergency department
remains controversial. The drug reduces swelling and helps minimize
secondary injury by reversing the intracellular accumulation of calcium,
reducing the risk for cord degeneration and ischemia.
- Steroid use has also been associated with severe pneumonia and sepsis. The
physician determines whether to prescribe methylprednisolone based on
assessment of the patient, past medical history, and diagnostic testing.
Nursing management in ICU:

1-Respiratory management:
- Closely monitor the patient’s respiratory rate, depth, and pattern, breath
sounds, cough strength, arterial blood gas (ABG) results and staying alert
for paradoxical breathing.
- Maintain continuous pulse oximetry; when possible, use end-tidal
capnography as part of routine monitoring.
- Intubation. Patients with respiratory failure require mechanical ventilation
- Provide adjunctive treatments, including chest physical therapy and
postural drainage, suctioning, bronchoscopy.
- An abdominal binder placed below the costal margin to support the
viscera can aid breathing

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2-Cardiovascular management:
- Maintain a mean arterial pressure (MAP) of 85 mm Hg or higher for 7 days
(an approach called hemodynamic push)
- Fluid resuscitation is accomplished by infusing intravenous fluids,
crystalloids, or blood.
- Early administration of blood enhances oxygenation and may minimize the
secondary ischemic injury to the spinal cord.
- Once the patient is cleared for mobilization, neurogenic
orthostatic hypotension may occur.:
- Such strategies as abdominal binder application, compression stockings,
compression wrappings for the lower extremities, and slow elevation of the
head of the bed may help reduce this risk.
- Peripheral vasoconstrictor medications like midodrine, and
mineralocorticoids like fludrocortisone can help.
- Increased salt intake can also help with volume expansion and help with
symptom control.
- Stimulation of the vasovagal reflex may lead to cardiac arrest,
requiring emergency atropine administration.
- -To prevent a systole episodes, hyper oxygenate the patient before turning or
suctioning (unless contraindicated).
- Cardiac pacing has been used in patients whose hypotension fails to
resolve over time or who require frequent doses of anticholinergic drugs.
3-Temperature dysregulation.
Inability to sweat or shiver (poikilothermia) affects the patient’s
temperature regulation and can worsen bradycardia. Nursing care include
the following:
- Monitor environmental temperature, as this can affect body temperature.

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- Therapeutic hypothermia involves the reduction of core body temperature,
by IV or regional (dural) cooling.
- Hypothermia management reduce nervous system metabolism, which is
thought to decrease the detrimental effects of secondary injury.
- However hypothermia may worsen bradycardia and hypotension. Provide
gentle rewarming and monitor core temperature continuously.
4-measures of Venous stasis prophylaxis includes:
- Immediate application of pneumatic compression sleeves, along with sub
therapeutic heparin or enoxaparin initiated 72 hours after the injury, once
the bleeding risk resolves.
- In cases of blood clot formation, the patient may receive an implantable
filter in addition to conventional anticoagulant therapy.
5-Autonomic Dysreflexia:
- Treatment is aimed at alleviating the noxious stimuli.
- Use rapid interventions, such as sitting the patient upright to induce
orthostasis (if possible)
- If symptoms persist, antihypertensive agents can be administered to reduce
blood pressure (fast-acting antihypertensive agents such as nifedipine).
6-GI management:
- Monitor the patient’s bowel sounds and abdominal distention at least every
4 hours.
- If indicated and ordered, insert a decompressive gastric tube to reduce
aspiration risk and restore diaphragm position and lung size to normal.
- The injury level determines whether the patient has a neurogenic (upper
motor neuron) or a neurogenic (lower motor neuron) bowel.

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- Neurogenic bowel is marked by loss of voluntary control of the external
rectal sphincter, tight reflexive sphincter tone, retained stool, and
constipation.
- To aid bowel regulation, the patient may need a bowel regimen of stool
softeners and a high-fiber diet along with low-volume enemas, glycerin.
- To reduce the risk of constipation-induced AD, perform a digital check of
the rectum for retained stool.
- A neurogenic bowel patients have a slow colonic transport time and lose
both voluntary control and reflexive sphincter tone.
- Fecal incontinence is common. Stool softeners, mini-enemas, and digital
stool removal may keep the rectum empty, reducing incontinence
frequency.
7- Genitourinary management:

A-Acute urinary retention:

- A patient in neurogenic shock experiences abrupt loss of voluntary muscle
control and reflexes, resulting in acute urinary retention.
- An indwelling urinary catheter must be placed to decompress the
bladder and allow close urinary output monitoring during the initial
resuscitation and critical management phases.
- The catheter stays place until the patient achieves hemodynamic stability,
B- SCI can cause neurogenic or a neurogenic bladder:
- Neurogenic bladder, the bladder is flaccid, reflex-initiated voiding may
occur when the patient has a full bladder.
- -The Credé method is more appropriate for a bladder that is flaccid
- A neurogenic bladder, voiding doesn’t occur, potentially causing overflow
urine leakage (incontinence). Bladder is spastic and will empty in response
to overstretching of the bladder wall

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 - Planned intermittent catheterization and Teach the patient how to self-
catheteriz can reduce incontinence.
- Emptying the bladder at regular intervals through intermittent
catheterization.
8-Musculoskeletal management:
- Muscle spasticity as spinal shock recedes and reflexes return.
- Nonpharmacological strategies include range-of motion exercises,
positioning techniques, weight-bearing exercises, electrical stimulation, and
orthoses or splinting to prevent loss of muscle length and contractures.
Pharmacologic therapy may include baclofen, benzodiazepines, alpha2-adrenergic
agonists, and regional botulism toxin or phenol injection.

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