TRAUMATIC BRAIN INJURY (TBI)

- Is a disruption in the normal function of the brain that can be caused by a blow, bump or jolt to
the head, the head suddenly and violently hitting an object or when an object pierces the skull
and enters brain tissue.

TYPES OF TRAUMATIC BRAIN INJURY

CONCUSSION caused by a bump, blow, or jolt to the head or by a hit to the body that causes the head
and brain to move rapidly back and forth.

CONTUSION bruising of the brain can be coup or contrecoup type.

Extra-axial Hematoma includes;

*EPIDURAL HEMATOMAS (EDH)
- usually results from bleeding from the middle artery and its branches or a fracture and its usually
acute.
-between dura mater and inner aspect of periosteum
-Period of loss consciousness and lucid interval
-ICP increases which individual develops headache, nausea, vomiting and focal neurologic symptoms
-Hematoma grows rapidly it can cause life threatening brain hernation.

*Subdural Hematomas (SDH)

-between dura mater and arachnoid mater
-Can result from the bleeding of a bridging vein and can be acute (w/in2days), subacute (2days-2wks) or
chronic (2wks or more). Bridging veins is very vulnerable to rapid acceleration and deceleration
-Brain atrophy and shrinkage
-Often time individual don’t remember traumatic events thus its important to consider SDH especially in
elderly with neurological symptoms.
-SDH in infants or child could be due to non-accidental trauma or child abuse
-Grows slower than EDH and tend to be more insidious
-ICP increases causing symptoms such as worsening headaches, nausea or vomiting, unsteady gait,
confusion, visual problems, slurred speech, cognitive impairment, seizures, dizziness and hemiparesis
-SDH large enough canlead to brain herniation, coma or death

-Morbidity and mortality is high thus treatment is prompt surgical hematoma evacuation.

SUBARACHNOID HEMORRHAGE
-Between arachnoid mater and pia mater
-Most common cause of SAH is head trauma while spontaneous SAH is ruptured aneurysm
-Less frequent cause of spontaneous SAH is arteriovenous malformation
-Most cases SAH progresses rapidly and individual complain of excruciating headaches also known
thunderclap headache descried as ‘worst headache of my life’
-Nuchal rigidity, seizures and symptoms of ICP like vomiting,vision changes and confusion

1
-Some individual w/ SAH develops electrolytes imbalances such as hyponatremia which result to SIADH
and cerebral salt wasting.

Intra-axial Injuries;
DIFFUSE AXONIAL INJURIES (DAI)
-This can underlie mild to moderate TBI and potentially results from any shearing, streatching or twisting
to the neuronal axons. Mainly seen at the junction of the gray and white matter.
-DAI leads to prolonged post-traumatic trauma define as more than 6 hours
-Often have lasting cognitive deficit such as memory loss problems with language.

Observing one of the following clinical signs constitutes alteration in the normal brain function:
•Loss of or decreased consciousness
•Loss of memory for events before or after the event (amnesia)
•Focal neurological deficits such as muscle weakness, loss of vision, change in speech
•Alteration in mental state such as disorientation, slow thinking or difficulty concentrating

Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain.
Mild cases may result in a brief change in mental state or consciousness. Severe cases may result in
extended periods of unconsciousness, coma, or even death.

SYMPTOMS •Breathing problems, slow pulse

Symptoms vary greatly depending on the severity •Slow breathing ratewith an increase in blood
of the head injury. They may include any of the pressure
following: •Ringing in the ears or changes in hearing
•Vomiting, lethargy, headache, confusion •Cognitive difficulties
•Paralysis, coma •Inappropriate emotional responses
•Loss of consciousness, dilated pupils •Speech difficulties (slurred speech, inability to
•Vision changes (blurred vision or seeing double, understand and/or articulate words)
unable to tolerate bright light, loss of eye •Difficulty swallowing
movement, blindness) •Body numbness or tingling
•Cerebrospinal fluid (CSF) (clear or blood-tinged) •Droopy eyelid or facial weakness
appear from the ears or nose •Loss of bowel control or bladder control
•Dizziness and balance concerns

CAUSES: •Physical violence

Causes of traumatic brain injury include:
•Car accidents
Causes of acquired brain injury include:
•Blows to the head
•Poisoning or exposure to toxic substances
•Sports injuries
•Infection
•Falls or accidents

2
•Strangulation, choking, or drowning •Aneurysms
•Stroke •Neurological illnesses
•Heart attacks
•Abuse of illegal drugs
•Tumors

ASSESSMENT 5. Irregular respirations

1. Disturbance in level of consciousness from 6. Cognitive deficit

slightly drowsy to unconscious.
7. Pupillary abnormality
2. Headache, vertigo, agitation, and restlessness.
8. Sudden onset of neurologic deficits
3. Cerebrospinal fluid leakage at ears and nose,
9. Otorrhea indicating posterior fossa skull fracture
which may indicate skull fracture.
10. Rhinorrhea indicating anterior fossa skul
4. Contusions about eyes and ears indicating skull
fracture.
fractures.

NURSING DIAGNOSIS

 Risk for injury related to complications of head injury.

 Acute pain related to altered brain or skull tissue.

DIAGNOSTIC EVALUATION

 CT identifies and localizes lesions, cerebral edema, and bleeding.

 Skull and cervical spine X-ray identify fracture and displacement.
 Complete blood count, coagulation profile, electrolyte levels, serum osmolarity, arterial blood
gases, and other laboratory tests monitor for complications.
 Neuropsychological test during rehabilitation phase determine cognitive deficits.

GLASGOW COMA SCALE

This 15-point test helps a doctor or other emergency medical personnel assess the initial severity of a
brain injury by checking a person's ability to follow directions and move their eyes and limbs. The
coherence of speech also provides important clues.

3
Abilities are scored from three to 15 in the Glasgow Coma Scale. Higher scores mean less severe injuries.

IMAGING TESTS

Computerized tomography (CT) scan. A CT scan can quickly visualize fractures and uncover evidence
of bleeding in the brain (hemorrhage), blood clots (hematomas), bruised brain tissue
(contusions), and brain tissue swelling.
 Magnetic resonance imaging (MRI). This test may be used after the person's condition
stabilizes, or if symptoms don't improve soon after the injury.

NURSING INTERVENTIONS

 Maintain ICP monitoring, as indicated, and report abnormalities.

 Maintain patent airway; assist with intubation and ventilatory assistance is needed.
 Turn the patient every 2 hours and encourage coughing and deep breathing.
 Apply firm pressure over puncture site for subdural trap, and observe for drainage and
dressing.
 Suction the patient as needed.
 Institute measures to prevent increased ICP or other neurovascular compromise.
 Feed the patient as soon as possible after a head injury and administer histamine-2 blockers
to prevent gastric ulceration and hemorrhage from gastric acid hypersecretion.
 If the patient is unable to swallow, provide enteral feedings after bowel sounds have
returned.
 Elevate the head of the bed after feedings, and check residuals to prevent aspiration.
 Monitor respiratory rate, depth, and pattern of respirations.

4
MEDICAL MANAGEMENT

 Maintain airway and ventilation

 Maintain cerebral perfusion pressure
 Prevent secondary injuries (by recognizing and treating hypoxia, hypercapnia, or hypoperfusion)
 Evaluate and manage for increased ICP
 Obtain urgent neurosurgical consultation for intracranial mass lesions
 Identify and treat other life-threatening injuries or conditions (if they exist)
 A relatively higher systemic blood pressure is needed:
 Increase in intracranial pressure
 Loss of autoregulation of cerebral circulation
 Priorities remain the same: the ABC also applies to TBI. The purpose is to optimize perfusion
and oxygenation.

NURSING MANAGEMENT

 Assess vitals
 Assess neurological injury
 Assess oxygenation and ventilation
 Observe pupils for signs of elevated intracranial pressure
 Assess ins and outs
 Check nose and ear for CSF leak
 Assess if the patient is able to sense or has pain
 Encourage coughing
 Provide stress ulcer and DVT prophylaxis
 Administer IV fluids
 Check labs (SIADH is common)
 Check the endotracheal tube for position and patency
 Suction the airways
 Provide skincare and pressure ulcer prophylaxis
 Provide a safe environment for the patient
 Administer medications as prescribed

TREATMENT

Medications, surgical and Rehabilitation

Medications may be used to help control symptoms.

 Sedation
 Pain relief
 Diuretics

5
  Anti-seizure medication
 Coma-inducing medications

Surgery may be necessary in some cases.

 Removing a hematoma
 Repairing a skull fracture
 Creating an opening in the skull

Rehabilitation

Most people who have had a significant brain injury will require rehabilitation. They may need to relearn
basic skills, such as walking or talking. The goal is to improve their abilities to perform daily activities

Rehabilitation specialists may include:

 Physiatrist
 Occupational therapist
 Physical therapist,
 Speech and language therapist
 Neuropsychologist
 Social worker or case manager
 Rehabilitation nurse
 Traumatic brain injury nurse specialist
 Recreational therapist
 Vocational counselor

TIPS FOR RECOVERY:

 Avoid activities that could cause another

blow or jolt to the head.
 Follow the instructions of healthcare
professionals.
 Do not take drugs that the physician has
not approved.
 Do not return to normal activities, including
driving and sports participation, until the
doctor agrees.
 Get plenty of rest.

6
PROGNOSIS

According to American Association of Neurological Surgeons (AANS) 2022;

•Patient with moderate head injuries fare less well. Approximately 60 percent will make a positive
recovery and an estimated 25 percent left with a moderate degree of disability.Death or a persistent
vegetative state will be the outcome in about 7 to 10 percent of cases. The remainder of patients will
have a severe degree of disability.

•The group comprised of severely head-injured patients has the worst outcomes. Only 25%-33% of
these patients have positive outcomes. Moderate disability and severe disability each occur in about a
sixth of patients, with moderate disability being slightly more common. About 33% of these patient do
not survive. The remaining few percent remain persistently vegetative.

ACUTE ISCHEMIC STROKE

- Acute ischemic stroke is a medical emergency caused by decreased blood flow to the brain,
which results in damage to brain cells. Acute ischemic stroke (AIS) is responsible for almost 90%
of all strokes. Acute ischemic stroke occurs when blood flow through a brain artery is blocked by
a clot, a mass of thickened blood. Clots are either thrombotic or embolic, depending on where
they develop within the body.
- A thrombotic stroke, the most common of the two, occurs when a clot forms within an artery in
the brain. An embolic stroke occurs when a clot or small piece of plaque (fatty deposit) breaks
off from elsewhere in the body, such as the heart, and travels through the bloodstream only to
become stuck in a narrower vessel in the brain.
- Almost half of all acute ischemic strokes are due to large vessel occlusion (LVO). An LVO is the
most severe and debilitating type of stroke as the clot occludes major arteries and prevents
blood flow to significant portions of the brain.

SIGNS AND SYMPTOMS INCLUDE:

 Trouble speaking and understanding your mouth may droop when you try to
what others are saying. You may smile.
experience confusion, slur words or
 Problems seeing in one or both
have difficulty understanding speech.
eyes. You may suddenly have blurred or
 Paralysis or numbness of the face, arm blackened vision in one or both eyes, or
or leg. You may develop sudden you may see double.
numbness, weakness or paralysis in the
 Headache. A sudden, severe headache,
face, arm or leg. This often affects just
which may be accompanied by
one side of the body. Try to raise both
vomiting, dizziness or altered
your arms over your head at the same
consciousness, may indicate that you're
time. If one arm begins to fall, you may
having a stroke.
be having a stroke. Also, one side of

7
  Trouble walking. You may stumble or  Face. Ask the person to smile. Does one
lose your balance. You may also have side of the face droop?
sudden dizziness or a loss of
 Arms. Ask the person to raise both
coordination.
arms. Does one arm drift downward? Or
Act FAST: is one arm unable to rise?

Seek immediate medical attention if you  Speech. Ask the person to repeat a
notice any signs or symptoms of a stroke, simple phrase. Is his or her speech
even if they seem to come and go or they slurred or strange?
disappear completely. Think "FAST" and do
 Time. If you observe any of these signs,
the following:
call 911 or emergency medical help
immediately.

RISK FACTORS

Many factors can increase the risk of stroke.  Personal or family history of stroke,
Potentially treatable stroke risk factors include: heart attack or transient ischemic attack

Lifestyle risk factors  COVID-19 infection

 Being overweight or obese Other factors associated with a higher risk of

stroke include:
 Physical inactivity
 Age — People age 55 or older have a
 Heavy or binge drinking
higher risk of stroke than do younger
 Use of illegal drugs such as cocaine and people.
methamphetamine
 Race or ethnicity — African Americans
Medical risk factors and Hispanics have a higher risk of
stroke than do people of other races or
 High blood pressure ethnicities.
 Cigarette smoking or secondhand  Sex — Men have a higher risk of stroke
smoke exposure than do women. Women are usually
 High cholesterol older when they have strokes, and
they're more likely to die of strokes
 Diabetes than are men.
 Obstructive sleep apnea  Hormones — Use of birth control pills
 Cardiovascular disease, including heart or hormone therapies that include
failure, heart defects, heart infection or estrogen increases risk.
irregular heart rhythm, such as atrial
fibrillation

PREVENTION

Many stroke prevention strategies are the same as strategies to prevent heart disease. In general,
healthy lifestyle recommendations include:

8
  Controlling high blood pressure  Eating a diet rich in fruits and
(hypertension) vegetables

 Lowering the amount of cholesterol  Exercising regularly; Drinking alcohol

and saturated fat in your diet in moderation, if at all

 Quitting tobacco use  Treating obstructive sleep apnea (OSA)

 Managing diabetes  Avoiding illegal drugs

 Maintaining a healthy weight

DIAGNOSIS

Your doctor may:

 Ask you or your family member about  Computed tomography (CT scan) uses
your risk factors, such as high blood X-rays to take clear, detailed pictures of
pressure, smoking, heart disease, and a your brain.
personal or family history of stroke.
 Computed tomography
 Ask about your signs and symptoms and angiography (CTA) uses a combination
when they began. of CT scanning, special computer
techniques, and dye injected into the
 Conduct a physical examination to
blood to produce images of blood
assess your mental alertness and your
vessels.
coordination and balance. He or she
may check for numbness or weakness in  Magnetic resonance imaging (MRI)
your face, arms, and legs; trouble uses magnetic fields and radio waves to
speaking and seeing clearly; and create detailed images that can show
confusion. subtle changes in neurological tissues.

 Look for signs of carotid artery disease,  Magnetic resonance

a common cause of ischemic stroke. A angiography (MRA) can record the
stethoscope can detect a whooshing pattern and velocity of blood flow
sound called a bruit, which may suggest through vascular lesions as well as the
changed or reduced blood flow due to flow of cerebrospinal fluid throughout
plaque buildup. the brain.

Your doctor may order one or more of the  Transcranial Doppler

following tests: ultrasound evaluates blood flow
through the brain by directing high-
 Cerebral angiography, also called
frequency sound waves through the
cerebral arteriography, uses an
skull at particular arteries. The resulting
injection of a water-soluble dye, called a
sound wave signals that bounce back
contrast agent, to highlight the affected
from blood cells are interpreted by a
area so that it can be seen on X-rays.

9
 computer to make an image of the Additional tests may include: carotid
speed of blood flow. ultrasound, carotid angiography,
electrocardiography (EKG), echocardiography,
and/or blood tests.

PROGNOSIS

- Early improvement and younger age suggest a favorable prognosis. About 50% of patients with
moderate or severe hemiplegia and most with milder deficits have a clear sensorium and
eventually can take care of their basic needs and walk adequately.

TRAUMATIC SPINAL CORD INJURY

What is Spinal Cord Injury?

Spinal cord injury (SCI) is defined as damage to the spinal cord that temporarily or permanently
causes changes in its function. SCI is divided into traumatic and non-traumatic etiologies.

Traumatic Spinal cord injury

- occurs when an external physical impact acutely damages the spinal cord. A traumatic spinal cord
injury can stem from a sudden, traumatic blow to your spine that fractures, dislocates, crushes, or
compresses one or more of your vertebrae.

Classification of SCI:

Complete SCI - damage occurring across the whole spinal cord width, leading to complete loss of
sensation and paralysis below the level of injury.

Incomplete SCI - the injury is spread across part of the spinal cord thereby only partially affecting
sensation or movement below the level of injury.

Paralysis from a Spinal Cord Injury can be referred to as:

Tetraplegia. Also known as quadriplegia, this means that your arms, hands, trunk, legs and pelvic
organs are all affected by your spinal cord injury.

Paraplegia. This paralysis affects all or part of the trunk, legs and pelvic organs.

10
EMERGENCY SIGNS AND SYMPTOMS
Emergency signs and symptoms of a spinal cord injury after an accident include:

 Extreme back pain or pressure in your neck, head or back

 Weakness, incoordination or paralysis in any part of your body
 Numbness, tingling or loss of sensation in your hands, fingers, feet or toes.Loss of bladder or
bowel control
 Difficulty with balance and walking
 Impaired breathing after injury
 An oddly positioned or twisted neck or back

Diagnosis

After any traumatic injury, first responders rapidly assess patients in the field and attempt
resuscitation in route to the hospital. During this period, the advanced trauma life support protocols
dictate initial care, which includes airway, breathing and circulation support, along with the
immobilization of the potentially injured and unstable spinal column using a rigid cervical collar and
backboard. Although individual hospital approaches vary, most patients with trauma will undergo a
gross neurological examination (which includes a voluntary motor and sensory examination of each limb
and a rectal examination) and spinal imaging (using, for example, X-ray or CT imaging) if a SCI is
suspected. Concerns on clinical examination or early radiographic imaging are followed by advanced
imaging and detailed neurological examinations.

Diagnostic Test: Imaging

Diagnostic tests for spinal cord injuries may include a CT scan, MRI or X-ray. These tests will help
the doctors get a better look at abnormalities within the spinal cord. Your doctor will be able to see
exactly where the spinal cord injury has accursed.

A complete neurological exam will be performed a few days after the injury. This length of time will
allow any swelling to subside, which will allow your doctor to diagnose the severity of the spinal cord
injury and predict the likelihood of recovery and the possible outcomes from treatment.

Management

 Restricting movement of the spine is recommended to prevent further damage to the spinal
cord, with the patient initially strapped to a backboard prior to further assessment or imaging.
Once initially stabilized, ensure appropriate pain management. Regular neurological
observations should be made.
 Conservative management includes a combination of bed rest, cervical collars, motion
restriction devices, and traction, followed by early mobilization and rehabilitation.

11
Surgical Management

The absolute indications for surgical management of a traumatic spinal cord injury are evidence of
a progressive neurological deficit or a dislocation-type injury to the spinal column (displaced and
unstable).

 Cervical spine surgery aims to realign the spine, decompress the neural tissue, and stabilise
the spine with internal fixation (screws, plates, cages)
 Thoracolumbar spine surgery typically involves spinal decompression, discectomy, spinal
fixation, or spinal cord simulation
 Physiotherapy and other specialist therapy input (e.g. speech and language or occupation
therapy) should be utilised early (as soon as deemed safe), as TSCI patients often require
extensive rehabilitation both as inpatient and outpatient. Goals of therapy need to be
discussed with the patient, to build a realistic rehabilitation plan.

SHOCK

Is defined as a state of cellular and tissue giving into TACHYCARDIA. The respiratory rate
hypoxia due to either reduced oxygen delivery, will increase to get more oxygen, so we see
increased oxygen consumption, inadequate tachypnea, and the body compensates with the
oxygen utilization, or a combination of these sympathetic nervous system to speed up the
processes. Shock is a critical condition where vital signs.
the body has decreased tissue perfusion
III. Progressive stage. The compensatory
eventually leading to organ failure and death.
mechanisms begin failing to meet tissue
The classic sign of shock is low blood pressure.
metabolic needs, and the shock cycle is
4 stages of shock: initial, compensatory, perpetuated. Now, a key sign to remember in
progressive, and irreversible. the progressive stage is cold & clammy skin.
This is an early sign that the body is lacking
I. Initial stage- cardiac output (CO) is decreased,
perfusion & getting worse not being able to
and tissue perfusion is threatened. There is too
compensate anymore. In the progressive stage,
little oxygen in the blood to feed the organs
cold and clammy skin is the priority.
resulting in anaerobic metabolism, meaning,
metabolism without oxygen BUT signs & IV. Irreversible stage. Shock becomes
symptoms are absent in this stage. unresponsive to therapy and is considered
irreversible. Basically meaning, death is
II. Compensatory- Almost immediately, the
imminent.
compensatory stage begins as the body’s
homeostatic mechanisms attempt to maintain
CO, blood pressure, and tissue perfusion. This is
Types of Shock
where the body is trying to compensate for that
low oxygen. So, the heart will pump faster 1. Cardiogenic Shock

12
2. Hypovolemic Shock Causes

3. Obstructive Shock Hypovolemic shock usually results from acute

blood loss- about one-fifth of the total volume.
4. Distributive Shock
 Internal fluid loss. Internal fluid losses
4a. Septic
can result from hemorrhage from a
4b. Neurogenic trauma like a gunshot or a knife injury
or even from surgery where we get too
4c. Anaphylactic much blood loss & even GI bleeding or
third-space fluid shifting in burn pts.
 External fluid loss. External fluid loss
2. Hypovolemic shock- reduced intravascular can result from severe bleeding or from
blood volume causes circulatory dysfunction severe diarrhea, diuresis, or vomiting.
and inadequate tissue perfusion. Vascular fluid  Inadequate vascular
volume loss causes extreme tissue volume. Inadequate vascular volume
hypoperfusion. leads to decreased venous return and
Pathophysiology cardiac output.

 Fluid loss. Fluid loss can either be an Whatever the cause, the signs & symptoms are
internal or external fluid loss. typically the same.
 Compensatory mechanism. The
resulting drop in arterial blood pressure
activates the body’s compensatory Clinical Manifestations
mechanisms in an attempt to increase Hypovolemic shock requires early recognition of
the body’s intravascular volume. signs and symptoms.
 Venous return. The diminished venous
return occurs as a result of the decrease  Clammy skin. The patient develops cool,
in arterial blood pressure. clammy, and pale skin. This is a priority
 Preload. The preload or the filling as mentioned before. This is seen in the
pressure becomes reduced. progressive stage & is indicating that
 Stroke volume. The stroke volume is the client is getting worse.
decreased.  Hypotension. Hypovolemic shock
 Cardiac output. Cardiac output is produces hypotension with narrowed
decreased because of the decrease in pulse pressure. Just like w/ any shock,
stroke volume. we see severely low BP, less than 90
 Arterial pressure. Reduced mean systolic.
arterial pressure follows as the cardiac  Tachycardia. The body compensates for
output gradually decreases. the decreased cardiac output by
 Compromised cell nutrients. As the pumping faster than normal, resulting
tissue perfusion decreases, the delivery in tachycardia. due to compensatory
of nutrients and oxygen to the cells is mechanisms to maintain the cardiac
decreased, which could ultimately lead output and perfusion.
to multiple organ dysfunction  Oliguria. There is oliguria or decreased
syndromes. urine output of less than 25ml/hour.

13
  Cognitive. The patient experiences return of the available circulating blood
decreased sensorium. volume to the legs.
 Rapid, shallow respirations. Due to the  Treat underlying cause. If the patient is
decrease in oxygen delivery around the hemorrhaging, efforts are made to stop
body systems, the respiratory system the bleeding or if the cause
compensates by rapid, shallow is diarrhea or vomiting, medications to
respirations. treat diarrhea and vomiting are
administered.
Assessment and Diagnostic Findings
 Redistribution of fluid. Positioning the
 Laboratory findings. There is elevated patient properly assists in fluid
potassium, serum lactate, and blood redistribution, wherein
urea nitrogen levels. a modified Trendelenburg position is
 Urine characteristics. The urine specific recommended in hypovolemic shock.
gravity and urine osmolality are
increased.
 Blood considerations. Decreased blood Pharmacologic Therapy
pH, partial pressure of oxygen, and
If fluid administration fails to reverse
increased partial pressure of carbon
hypovolemic shock, the following are given:
dioxide.
 SpO2 sensor should be placed on the  Vasoactive drugs. Vasoactive drugs that
forehead instead of the extremities prevent cardiac failure are given.
since there will be a lack of perfusion. Initially, the vital signs will improve
from the fluid or volume expansion but
it won’t last so that’s why we do
Medical Management vasoactive drugs: norepinephrine,
phenylephrine, epinephrine, and
Emergency treatment measures must include vasopressors. This is definitely needed
prompt and adequate fluid and blood to maintain blood pressure for the long
replacement to restore intravascular volume term.
and raise blood pressure.
 Desmopressin (DDAVP). Desmopressin
 Volume expansion. Saline or lactated is administered for diabetes insipidus.
Ringer’s solution, possibly plasma  Antidiarrheal drugs. If dehydration is
proteins or other plasma expanders, due to diarrhea, antidiarrheal
may produce adequate volume medications are administered.
expansion until whole blood can be  Antiemetics. If the cause of diarrhea is
matched. vomiting, antiemetics are given.
 Pneumatic antishock garment. A
pneumatic antishock garment
counteracts bleeding and hypovolemia Nursing Interventions
by slowing or stopping arterial bleeding;
Nursing care focuses on assisting with
by forcing any available blood from the
treatment targeted at the cause of the shock
lower body to the brain, heart, and
and restoring intravascular volume.
other vital organs; and by preventing

14
  Safe administration of blood. It is  Monitor weight. Monitor daily weight
important to acquire blood specimens for sudden decreases, especially in the
quickly, to obtain a baseline complete presence of decreasing urine output or
blood count, and to type and active fluid loss.
crossmatch the blood in anticipation of  Monitor vital signs. Monitor vital signs
blood transfusions. of patients with deficient fluid volume
 Safe administration of every 15 minutes to 1 hour for the
fluids. The nurse should monitor the unstable patient, and every 4 hours for
patient closely for cardiovascular the stable patient.
overload, signs of difficulty of breathing,  Oxygen administration. Oxygen is
pulmonary edema, jugular administered to increase the amount of
vein distention, and laboratory results. oxygen carried by available hemoglobin
in the blood.

Obstructive Shock  Tachycardia (fast heart rate).

 Altered consciousness.-Going into shock
can cause an acquired brain injury by
Obstructive shock is a condition that prevents reducing the amount of oxygen-rich
blood and oxygen from getting to your organs. blood that reaches the brain. Without
You need immediate treatment of the problem blood and oxygen, the brain quickly
that caused this emergency, such as a blood clot begins deteriorating. Neural cells die,
or collapsed lung. and a shock acquired brain injury (ABI)
can occur.
With any type of shock, your entire body can’t
 Very little pee output. Maliit nalang ang
get enough blood flow, which means it can’t get
blood na mafigilter Yung waste para
enough oxygen. With obstructive shock,
maging urine.
something is obstructing or getting in the way of
 Cool, clammy skin.- The blood plays a
blood going into and out of your heart or great
role in temperature regulation. It
vessels (major blood vessels connected to your
distributes heat throughout the body,
heart). This obstruction can quickly lead to a
from the core to the surface and vice
huge drop in blood pressure and the amount of
versa. By changing the blood flow to the
blood your heart is able to pump. The shortage
skin, the body can control heat
of oxygen this creates affects all of your organs..
exchange at its surface with its
surrounding
 Subcutaneous emphysema (air under
SYMPTOMS AND CAUSES your skin).
What are the symptoms?  Chest or abdominal pain.

Symptoms can be similar to cardiogenic shock What causes obstructive shock?

symptoms. Obstructive shock symptoms
Causes of obstructive shock include:
include:
 Tension pneumothorax (collapsed lung).
 Unusually fast breathing.
 Hypotension (low blood pressure).

15
  Vena cava compression syndrome (a  Possible obstructive shock treatments
large blood vessel that gets include:
compressed).  Removing an embolism with surgery or
 Pulmonary (lung) compression a catheter.
syndrome.  Replacing a severely narrowed aortic
 High-PEEP (positive end-expiratory valve.
pressure) ventilation (pressure in your  Reducing heart muscle wall thickness,
airways after the ventilator exhales). either with surgery or catheter-based
 Tumors. alcohol ablation.
 Thromboembolism (clot) in the  Dissolving a blood clot.
pulmonary artery.  Draining or relieving a pericardial
 Pericardial tamponade (excess fluid tamponade or tension pneumothorax.
around your heart compresses it).  Adjusting your ventilation if needed.
 Aortic dissection (a rip in your aorta).  Changing your body position for vena
 Aortic stenosis (the opening to your cava compression syndrome.
aortic valve gets narrow).  Decompressing high lung pressures with
 Hypertrophic a needle or tube.
cardiomyopathy (thickened heart
What medications are used?
muscle causes obstruction of flow out
of your heart).  Your provider may give you:
 Constrictive pericarditis (the sac around  IV crystalloid fluids (such as saline).
your heart gets thick).  Norepinephrine (Levophed®).-
norepinephrine increases heart rate
DIAGNOSIS AND TESTS
and blood pumping from the heart. It
How is obstructive shock diagnosed? also increases blood pressure and helps
break down fat and increase blood
 Your healthcare provider will do a
sugar levels to provide more energy to
physical exam that includes listening to
the body.
your heart and lungs with a
 Vasopressin (Vasostrict®).- known to
stethoscope. A quick diagnosis is
regulate blood pressure, blood
important because obstructive shock
osmolality, and blood volume.
gets worse quickly.
 Phenylephrine (Vazculep® or
 Ultrasound.
Biorphen®).-used for the temporary
 Echocardiogram.
relief of congestion or stuffiness in the
 Computed tomography (CT).
nose caused by hay fever or other
 Electrocardiogram (EKG).
allergies, colds, or sinus trouble. It may
MANAGEMENT AND TREATMENT also be used in ear infections to relieve
congestion
How is obstructive shock treated?  Blood products (red blood cells,
 After giving you IV fluids and checking plasma).
your blood pressure and oxygen level,
your healthcare provider will need to
treat the cause of your obstructive
shock.

16
 study lead author Robert Cohn, MD,
MBA.

Distributive Shock
The major allergens in peanuts are generally
Distributive shock or vasodilatory shock is the
considered Ara h 1 and Ara h 3 that are
type of shock healthcare providers see most
members of the cupin superfamily of proteins,
often. Septic shock from sepsis makes up the
and Ara h 2 and Ara h 6 that are members of
largest number of cases, but people also get
the prolamin superfamily
distributive shock from severe allergic reactions
or asthma attacks. Quick treatment is very Neurogenic shock (from a spinal cord injury that
important, as it gives you the best odds of has damaged your nervous system). Example: A
survival. diving accident that injures your spinal cord and
leads to neurogenic shock.
What is distributive shock?

Distributive shock or vasodilatory shock is a

medical emergency where your body can’t get SYMPTOMS AND CAUSES
enough blood to your heart, brain and kidneys.
 Skin rash.
This happens because your blood vessels are
 Fast heart rate and breathing.
extremely dilated (flaccid or relaxed), which
brings down your blood pressure and cuts down  Low blood pressure.
on how much blood can get to your organs.  Warm arms and legs.
Often the small blood vessels (capillaries) are  Skin that starts out warm and then
leaky in distributive shock, resulting in some turns cold and clammy.
fluid loss from the circulation.  Fever.
 Chills.
You need to get treatment as soon as possible  Pain in your belly.
for vasodilatory shock.  Confusion.
 Cough.
 Shortness of breath.
The three types of distributive shock are:  Nausea.
Septic shock (from a bacterial infection).  Throwing up.
Example: A serious infection complication  Pain when trying to pee.
called sepsis that gets so bad it leads to septic What causes distributive shock?
shock....
Distributive shock causes include:
 Anaphylactic shock (from an allergic
reaction or asthma attack). Example:  Sepsis (from a bacterial infection).
An allergic reaction to peanuts that  Anaphylaxis (from nut allergies or
leads to anaphylactic shock. Many of asthma).
the respiratory symptoms of peanut  Burns.
allergy can mirror those of an asthma  Pancreatitis.
attack, and vice versa. Examples of  Toxic shock syndrome.
those symptoms include shortness of  Spinal cord injury.
breath, wheezing and coughing," said  Endocrine disorders.

17
  Adrenal insufficiency (less common). treatment. You may need a ventilator to
 Capillary leak syndrome (less common). help you breathe if you’re having
 Drug overdose of medicine that dilates trouble breathing on your own.
your blood vessels (less common).
What medications are used?
DIAGNOSIS AND TESTS
Depending on the cause of your distributive
How is distributive shock diagnosed? shock, your provider will give you the following
medicines:
 Your provider will want a physical exam
and medical history. Often, someone in  Vasopressors
shock may not be able to speak for (epinephrine, vasopressin, norepinephri
themselves. A loved one can tell your ne or phenylephrine) to raise your
provider if you have an allergy or have blood pressure.
had anaphylaxis in the past. Knowing  Antibiotics if there’s an infection.
what medicines or drugs you’re taking  Antihistamines if you’ve had an allergic
will help your provider with a diagnosis, reaction.
as well.  Steroids for an allergic reaction or
severe sepsis.
What tests will be done to diagnose
 Albuterol (such as Accuneb® or
distributive shock?
Proair®HFA) if your shock is due to an
Your healthcare provider will order the asthma attack.
following tests, some of which may be able to
Side effects of the treatment
be brought to your bedside:
Side effects from vasopressors include:
 Blood tests.
 Electrocardiogram (EKG).  Abnormal heart rhythm (arrhythmia).
 Chest X-ray.  Anxiety.
 Ultrasound of the heart, lungs and belly.  Collection of fluid in your lungs
(pulmonary edema).
 Chest pain.
MANAGEMENT AND TREATMENT  Coronary artery narrowing, which can
cause a heart attack.
How is distributive shock treated?
 Antibiotics can cause nausea and
 Your healthcare provider will give you diarrhea. Albuterol can make you feel
IV fluids, like saline. Next, they will give nervous, dizzy or sick to your stomach.
you medicines to address the cause of Antihistamines can make you sleepy or
your vasodilatory shock. Then, they may dizzy. They can also give you a
give you some nourishment (probably headache or fast heart rate.
through a tube feeding).
Nursing Diagnosis
 You’ll be in the intensive care unit (ICU)
after most likely starting out in the  Tachypnea, tachycardia
emergency room. Your provider will  Low blood pressure
continue to check your vital signs and  Urine output is low or none
watch for side effects of your  Edema

18
  Diaphoresis leak. Historically, this is associated with both
 Altered mental status vaginal and nasal tampon use.
 Fever
Neurogenic shock classically occurs in cases of
 Abnormal heart rate
trauma involving the cervical spinal cord. The
 Decreased oxygenation
sympathetic nervous system is damaged
 Presence of rales and crackles
resulting in a decreased adrenergic input to the
Causes blood vessels and heart, causing vasodilation
with resultant hypotension and a paradoxical
The most common causes of distributive shock bradycardia.
in the emergency department are sepsis and
anaphylaxis. In cases of trauma, neurogenic The distributive shock from adrenal
shock should also be on the differential. Other insufficiency occurs due to decreased alpha-1
less common causes of distributive shock receptor expression on arterioles secondary to
include adrenal insufficiency and capillary leak cortisol deficiency, which results in vasodilation.
syndrome. Drug overdose or toxicity should This is seen in patients on chronic steroids that
always be considered, particularly potent are stopped suddenly.
vasodilators such as calcium channel blockers
Capillary leak syndrome, while rare, should be
and hydralazine.
considered in the edematous patient with
Distributive shock as a result of sepsis occurs distributive shock. It occurs due to low blood
due to a dysregulated immune response to albumin. Decreased oncotic pressure leads to
infection that leads to systemic cytokine release fluid loss from the blood into the interstitium.
and resultant vasodilation and fluid leak from
Nursing Management
capillaries. These inflammatory cytokines can
also cause some cardiac dysfunction, called  Observe vitals
septic cardiomyopathy, which can contribute to  Assess mental status
the shock state.  Monitor Is and outs
 Administer medications as ordered
In anaphylaxis, the patient typically has a
 Ensure prophylaxis against DVT and
history of previous exposure to an antigen,
stress ulcer
although this is not required, with resulting IgE
 Check labs, esp BUN and creatinine
formation to that antigen. These IgE molecules
 Check for peripheral perfusion by
then attach to the surface of mast cells in the
monitoring skin color, warmth, and
tissues and basophils in blood. Consequent
pulses
exposure to the same antigen results in the IgE-
 Provide nutrition
mediated release of histamine from mast cells
and basophils, leading to systemic vasodilation  Ensure patient is comfortable and pain-
and capillary fluid leak. free
 Check blood glucose frequently is
Toxic shock syndrome should be considered in patient is diabetic
distributive shock. This disease is caused by  Make sure the patient is seen by
Staphylococcus aureus and group A streptococci different consultants
exotoxins that stimulate systemic cytokine  Check all IV sites for redness and
release with resulting vasodilation and capillary discharge

19
 Medical Management

Septic shock The current treatment of septic shock and

sepsis include identification and elimination of
- Since the ability of the body to provide
the cause of infection.
oxygen and nutrients is interrupted, the
heart compensates by pumping faster.  Fluid replacement therapy. The therapy
- Hypotension occurs because of is done to correct the tissue
vasodilation. hypoperfusion, so aggressive fluid
- To compensate for the decreased resuscitation must be implemented.
oxygen concentration, the patient tends  Nutritional therapy. Aggressive
to breathe faster, and also to eliminate nutritional supplementation is critical in
more carbon dioxide from the body. the management of septic shock
- The inflammatory response is activated because malnutrition further impairs
because of the invasion of pathogens. the patient’s resistance to infection.
- Decreased urine output. The body
Nursing Management
conserves water to avoid undergoing
dehydration because of the Nurses must keep in mind that the risks of
inflammatory process. sepsis and the high mortality rate associated
- Changes in mentation. As the body with sepsis, severe sepsis, and septic shock.
slowly becomes acidotic, the patient’s
mental status also deteriorates.  Nursing Assessment. Assessment is one
- Elevated lactate level. The lactate level of the nurse’s primary responsibilities,
is elevated because there is and this must be done precisely and
maldistribution of blood. diligently.
 Signs and symptoms. Assess if the
Prevention patient has positive blood culture,
Before sepsis could invade a patient’s body, it is currently receiving antibiotics, had an
better to prevent its occurrence here are some examination or chest x-ray, or has a
ways to prevent sepsis and septic shock. suspected infected wound.
 Signs of acute organ dysfunction. Assess
Assessment and Diagnostic Findings for presence of hypotension,
tachypnea, tachycardia, decreased
 Early assessment and diagnosis of the
urine output, clotting disorder, and
infection must be established to avoid
hepatic abnormalities.
its progression.
 Blood culture. To identify the Diagnosis
microorganism responsible for the
disease, a blood culture must be Sepsis can affect a lot of body systems and even
performed. cause their failure, so diagnosis is an important
part of the process to establish the presence of
 Liver function test. This should be
sepsis.
performed to detect any alteration in
the function of the liver.  Risk for deficient fluid volume related to
 Blood studies. Hematologic test must massive vasodilation.
also be performed to check on the  Risk for decreased cardiac output
perfusion of the blood. related to decreased preload.

20
  Impaired gas exchange related to hemodynamic status, fluid intake and
interference with oxygen delivery. output, and nutritional status.
 Risk for shock related to infection.
Evaluation
Planning & Goals
After implementation of the interventions, the
Healthcare team members should be prepared nurse must evaluate their effectiveness.
with a care plan for the patient for a more
 Patient displayed hemodynamic
systematic and detailed achievement of the
stability.
goals.
 Patient verbalized understanding of the
 Patient will display hemodynamic disease process.
stability.  Patient achieved timely wound healing.
 Patient will verbalize understanding of  Discharge and Home Care Guidelines
the disease process.  Even after discharge, the patient must
 Patient will achieve timely wound still be taught how to establish home
healing. and community care regimen.
 Prevent shock episodes. The nurse
Nursing Interventions
should instruct the patient and the
Nursing interventions pertaining to sepsis family strategies to prevent shock
should be done timely and appropriately to episodes through identifying the factors
maximize its effectivity. implicated in the initial episodes.
 Instructions on assessment. The patient
 Infection control. All invasive and the family should be taught about
procedures must be carried out with assessments needed to identify the
aseptic technique after careful hand complications that may occur after
hygiene. discharge.
 Collaboration. The nurse must  Treatment modalities. The nurse must
collaborate with the other members of teach the patient and the family about
the healthcare team to identify the site treatment modalities such as
and source of sepsis and specific emergency administration of
organisms involved. medications, IV therapy, parenteral or
 Management of fever. The nurse must enteral nutrition, skin care, exercise,
monitor the patient closely for and ambulation.
shivering.
 Pharmacologic therapy. The nurse Documentation Guidelines
should administer prescribed IV fluids
 Proper documentation must be
and medications including antibiotic
established both for legal protection
agents and vasoactive medications.
and data organization.
 Monitor blood levels. The nurse must
 Document individual risk factors.
monitor antibiotic toxicity, BUN,
 Document assessment findings.
creatinine, WBC, hemoglobin,
 Document results of the laboratory
hematocrit, platelet levels, and
tests and diagnostic studies.
coagulation studies.
 Document plan of care and teaching
 Assess physiologic status. The nurse
plan.
should assess the patient’s

21
  Document client’s responses to
treatment, teaching, and actions
performed.

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME

Content may lead to multiple organ failure and
shock.
1. Definition
2. Criteria of SIRS
3. Causes
4 Criteria of SIRS (Systemic Inflammatory
4. Risk Factors
Response Syndrome)
5. Pathophysiology
6. Complications 1. Body temperature over 38 or under 36
7. Treatment degrees Celsius.
8. Nursing Care
9. Patient Monitoring 2. Heart rate greater than 90
beats/minute
SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME 3. Respiratory rate greater than 20
breaths/minute or partial pressure of
 Also called SIRS. CO2 less than 32 mmHg
 A serious condition in which there is 4. Leukocyte count greater than 12000 or
inflammation throughout the whole less than 4000 /microliters or over 10%
body. It may be caused by a severe immature forms or bands.
bacterial infection (sepsis), trauma, or
pancreatitis. It is marked by fast heart NOTE: SIRS occurs when at least two of
rate, low blood pressure, low or high the following
body temperature, and low or high criteria are met.
white blood cell count. The condition

CAUSES

SIRS describes the host response to a critical illness of infectious or non-infectious cause such as:

22
 INFECTIOUS CAUSE NONINFECTIOUS CAUSE

 Bacterial sepsis
 Burns
 Burn wound infections
 Dehydration
 Septic arthritis
 Pancreatitis
 Nosocomial pneumonia
 Pancreatitis
 Community-acquired pneumonia
 Transfusion reactions
 Influenza
 Cirrhosis
 Urinary tract infections (male and
 Electrical injuries
female)
 Hemorrhagic shock

 Hematologic malignancy

RISK FACTORS

 Preoperative high heart rate

 Low albumin levels

 Postoperative intensive care unit (ICU) Admission

PATHOPHYSIOLOGY OF SEPSIS

Sepsis typically develops following infection or an inflammatory insult that is not contained and
cleared by the host. The dysregulation of the inflammatory response leads to disruption and damage to
the host immune system and several cell types. Endothelial and epithelial cells constitute an important
barrier in the containment of infection and inflammation. Disruption of the endothelial and epithelial

23
barrier could allow further dissemination of infection. Widespread cellular and immune dysfunction
could then propagate resulting in organ failure, eventually resulting in an irrecoverable state.

COMPLICATIONS 2. Antimicrobial Therapy

Administration of IV antibiotic therapy
 Respiratory failure, acute respiratory
should be initiated as soon as possible
distress syndrome(ARDS), and
(within 1 hour) after suspicion or
nosocomial pneumonia
confirmation of sepsis.
 Renal Failure

 Stress Ulcers 3. Infectious Source Control

Diagnosing the source of infection is
 Gastrointestinal Bleeding critical to patient outcome because
 Anemia stabilization requires source control.
Identifying the source of infection
 Electrolyte Abnormallities involves either medical or surgical
intervention.
 Hyperglycemia

4. Pain Management
TREATMENTS Sepsis/SIRS can be painful disease
processes, and therefore pain
1. Fluid Resuscitation
assessment and control need to be part
Aggressive fluid resuscitation is
of the treatment and nursing care.
necessary to restore circulatory status
(e.g., provide cardiovascular support,
maintain adequate tissue oxygen 5. Nutrition
delivery and perfusion) and maintain Nutrition is often overlooked as part of
hemodynamic stability. As such, the care for septic patients. However,
fluid resuscitation options include nutritional support is necessary for
isotonic crystalloids, hypertonic recovery from all disease processes and
crystalloids, synthetic colloids, and should be instituted for every patient.
vasopressor therapy.

24
NURSING CARE

SIRS/sepsis patients require intensive, dedicated nursing care and close monitoring during the
recognition, stabilization, and hospitalization periods.:

 Fluid balance  Gastrointestinal motility and integrity

 Albumin/oncotic pull  Nutrition

 Mentation/level of consciousness  Immune status (antibiotics)

 Heart rate/contractility/rhythm  Drug dosage and metabolism

 Blood pressure/perfusion  Pain control

 Oxygenation and ventilation  Wound care and bandages

 Body temperature  Nursing care

 Electrolytes and acid–base  Tender loving care

 Glucose  Coagulation

 Renal function  Red blood cells and hemoglobin

PATIENT MONITORING

 Assessment of vital signs every 2 to 10  SIRS/sepsis patients to require

minutes during initial stabilization and continuous electrocardiography
every 1 to 4 hours during monitoring and frequent blood pressure
hospitalization. measurement

25
  Urinary catheters require care every 6
to 8 hours to prevent a secondary
infection.

 Postoperative patients may have wound

drains that need to be quantified and
maintained.

 Pain scoring

MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)

Immediate type(primary): Dysfunction/Failure
occurring simultaneously in two or more organs
● Multiple organ dysfunction syndrome
due to primary disease.
(MODS), also known as multiple organ
failure (MOF), total organ failure (TOF) Delayed type(secondary): Dysfunction occurred
or multisystem organ failure (MSOF). in one organ other organs sequentially fail

● Multiple organ dysfunction syndrome Accumulation type: Dysfunction is cause by

(MODS) is a systemic, dysfunctional chronic disease. It is irreversible
inflammatory response that requires
CAUSES
long intensive care unit (ICU) stay.
Multiple organ dysfunction syndrome is •Initial Injury: Almost any disease that results in
the clinical consequence of a tissue injury may result in MODS examples
dysregulated inflammatory response, below:
triggered by clinically diverse factors
with the main pillar of management •Sepsis; Major trauma; Burns; Pancreatitis;
being invasive organ support. Aspiration syndromes; Extracorporeal
circulation (e.g. cardiac bypass); Multiple blood
● MODS results from SIRS and is the transfusion; Ischaemia–reperfusion injury;
failure of several interdependent organ Autoimmune disease; Heatinduced illness;
systems. SIRS is a systemic Eclampsia; Poisoning/toxicity
inflammatory response to a variety of
insults including infection, ischemia, SYMPTOMS
infarction, and injury, it leads to ● The patient may display some of the
disorders of microcirculation, organ following symptoms depending on
perfusion and finally secondary organ which organs are affected:
dysfunction.
● An altered mental state;
Classification of MODS

26
 ● A decrease in renal perfusion (decrease NURSING MANAGEMENT
in urine output);

● Respiratory deterioration;
Aim: Supporting the patient and monitoring
● A decrease in cardiac function; organ perfusion until primary organ insults are
halted.
● Deranged metabolic status;

● A compromised fluid balance;

1. Promoting Communication
● Pale, clammy, peripherally cool skin
and faint pedal pulses; and •A decrease ● Encourage frequent and open
in cardiac output (e.g. low blood communication about
pressure, arrhythmia) treatment modalities.

TREATMENT 2. Promoting Home, Community-Based, and

Transitional Care:

● Educating Patients About Self-

● Identifying and treating the underlying
Care
causes, comorbidities or complications;

● Fluid resuscitation to increase

perfusion

● Support care and monitoring:

Multi-organ support;

Mechanical or non-invasive ventilation;

Maintaining fluid homeostasis; and

Renal replacement therapy.

COLLABORATIVE MANAGEMENT

● Prevention and treatment of infection

● Maintenance of tissue oxygenation

● Nutritional and metabolic support

● Appropriate support of individual failing

organs

27