exam3

Spinal cord injury Ch 60- page 1403-1421 '

Etiology:

primary injury

- due to cord compression by bone displacement, interruption of blood supply, traction from pulling on cord - penetrating trauma (gun shot wound / stab wound) —> tearing and transection
- the initial mechanism disruption of axons as a result of stretch / laceration (primary injury)

Etiology: secondary injury

- within 24 hours: permanent damage may occur because of edema (secondary to inflammatory response) - extent of damage / prognosis of recovery most accurately determined 72 hours or more after injury.
- greatest improvement occurs in first 3-6 months following injury

Spinal Shock Neurogenic Shock

- characterized by: decreased reflexes, loss of sensation, absent thermoregulation (unable to self regulate), flaccid paralysis below level of injury, absent rectal sphincter tone / reflex
- lasts days to weeks and may mask post-injury neurologic function
- temporary

- characterized by: hypotension and bradycardia

- loss of SNS (sympathetic nervous system) innervation - peripheral vasodilation
- venous pooling
- decreased cardiac output

- T6 or higher injury (cervical or thoracic)
- results from loss of vasomotor tone due to injury and is characterized by hypotension / bradycardia

S&S: hypotension (decreased BP), bradycardia (slow HR), warm / dry extremities, peripheral vasodilation / venous pooling, polkilothermia (adapts room temperature), decreased CO (with cervical or high thoracic injury)

Classification of SCI

- mechanism of injury - flexion

- hyperextension
- flexion rotation: most often contributes to severe neurologic deficits. Most unstable because ligaments

that stabilize spine get torn - extension rotation
- compression

- level of injury
- skeletal (most common) vs. neurologic
- may be: Cervical, thoracic, lumbar, sacral - tetraplegia (quadriplegia)
- paraplegia

- degree of injury
- complete: total loss of sensory and motor function below the level of injury
- incomplete (partial): mixed loss of voluntary motor activity and sensation, some tracts intact — degree depends on level of injury and specific nerve damage tracts —

Sensory deprivation

- secondary to absent sensations
- stimulate patient above level of injury
- conversation, music, and interesting foods
- prism glasses to read / watch TV if HOB must stay flat.
- help patient avoid withdrawing from the surrounding environment —> depression is a common problem.

Pain management

- musculoskeletal nociceptive pain:

— antiinflammatory drugs: Ibuprofen (Motrin)

— opioids: morphine

- visceral nociceptive pain (needs imaging to dx cause) - neuropathic (nerve) pain:

— gabapntin (neurotoin), pregabalin (lyrica) — teach about pain triggers and relaxation therapy

Spinal cord injury Ch 60- page 1403-1421 '

Reflexes

Autonomic dysreflexia (Autnonimc hyperreflexia)

- return of reflexes may complicate rehab - hyperactive

- exaggerated response
- penile erections
- spasms (can range from twitching to convulsions)

- antispasmodic drugs

— baclofen (lioresal)
— dantrolene (dantrium) — tizanidine (zanaflex)

- massive uncompensated cardiovascular reaction mediated by sympathetic nervous system (SNS)
- SNS responds to stimulation of sensory receptors — parasympathetic nervous system is unable to

counteract these responses
- severe hypertension and bradycardia

- T6 or above
- most common precipitating factor is distended bladder or rectum
- manifestations: hypertension (up to 300 systolic), throbbing headache, bradycardia (30-40 bpm), diaphoresis above level of injury, piloerection (goose bumps), flushing of skin, blurred vision / spots in visual field, nasal congestion, anxiety, nausea
- nursing interventions: (1) elevate HOB to sit upright and lower legs. (2) notify HCP. (3) assess for / remove cause

— monitor / treat BP. If persists: administer rapid onset / short duration agents —> nitroglycerine, hydralazine, nitroprusside

Spasticity

- can be beneficial and undesirable
- ashworth / modified ashworth scale used to grade - treatments:

- ROM exercises
- antispasmodic drugs

— Tizanidine (Zanaflex)
— Dantrolene (Dantrium) — Baclofen (lioresal)
— botulinum toxin injections

-can be given to treat severe spasticity

Brain death

Brain death determination

F- irreversible cessation of circulatory and respiratory functions
OR
- irreversible cessation of all functions of the entire brain, including the brain stem

- 1980-81 the uniform determination of death act (became a law in 1981

3 cardinal findings-
- irreversible coma or unresponsiveness of known cause - absence of brainstem reflexes
- apnea

- patient must be comatose
- pupils must be non-reactive
- corneal reflex must be absent
- gag and cough reflex must be absent
- no response to painful stimuli
- oculocephalic reflex must be absent
- oculovestibular reflex must be absent
- spontaneous respirations must be absent - after atropine, HR should not incrase

Must be excluded:
- sedation
- neuromuscular blockade (paralysis) - shock
- hyperthermia
- metabolic in-balances

- neuro check must be completed after 6 hours
- time of death must be recorded at the time that the brain death is declared.

Uniform determination of death act

Clinical examination

Clinical evaluaition

Diagnostics (Done after in addition to neuro exam)

- transcranial doppler: checks cerebral blood flow — consistent with brain death - somatosensory evoked potentials: stimulates peripheral nerves (touch)
- EEG: monitors electrical activity.
- cerebral blood flow studies

Communications

- use the term dead as opposed to brain death to prevent family from thinking the rest of the body can continue to live - discussion of brain death is SEPARATE from that of organ donation

- completed by a CORE representative that contacts the family to avoid conflict of interest of the nurse.
** hospitals can get a fine if a nurse doesn’t call CORE for any death or impending death, you must call and document that you called.

-

- most common inflammatory conditions of the brain and spinal cord:

Inflammatory Brain Disorders

Overview

(Slide 2)

Brain abscess

- brain abscesses
- meningitis (inflammation of the meninges that surround the brain and spinal cord) - encephalitis (inflammation of the brain itself)

- 10 to 30 % mortality rate — higher in older patients
- 19 % of those who recover long term neurologic deficits among survivors (including hearing loss)

- pus within the brain tissue

Bacterial

- direct extension from an ear, tooth, mastoid, or sinus infection is primary cause.
- other causes include spread from distant site: pulmonary infection, bacterial endocarditis, skull fx, prior brain

trauma or surgery.
- primary infective organisms: streptococci / staphylococcus aureus
- manifestations (similar to meningitis / encephalitis): headache, fever, N&V - signs of increased ICP: drowsiness, confusion, seizures

- focal symptoms reflect local area of abscess
example: visual field defects or psychomotor seizures are common with a temporal lobe abscess. Whereas, an occipital abscess may be accompanied by visual impairment and hallucinations

- primary treatment: antimicrobial therapy, symptomatic treatment for other manifestations, and the abscess may need drained or removed if drug therapy isn’t effective.

- acute inflammation of meningeal tissue surrounding the brain and spinal cord.

meningitis (BAD- medical emergency)

- usually occurs in fall, winter or early spring and is often secondary to viral respiratory disease / illness
- older adults who are debilitated are more often affected than the general population. College students living in dorms and individuals living in institutions (prisoners) have a high risk for contracting meningitis.
- untreated bacterial meningitis has a mortality rate of near 100 % and must be reported to the CDC.

Etiology / pathophysiology: - leading causes:

— streptococcus pneumoniae
— neisseria meningitidis (has at least 13 subtypes, with 5 of them [A, B, C, Y, W] causes most cases)

- enter CNS thru upper respiratory tract or bloodstream

- may enter thru skull wounds or fractured sinuses - inflammatory response

- increased CSF production
- purulent secretions spread to other areas of the brain thru CSF - cerebral edema and increased ICP becomes problematic

- if process extends into parenchya or if concurrent encephalitis is present
- KEY SIGNS: fever, severe headache, nausea, vomiting, NUCHAL RIGIDITY, coma (associated with poor prognosis and occurs in 5-10 % of cases) diabetes

-

Inflammatory Brain Disorders

Bacterial meningitis- continued

Kernig's sign (Knees)

Clinical manifestations- photophobia, decreased LOC, signs of increased ICP (seizures occur in 1/3 of cases, headaches get worse, vomiting and irritability may occur), skin rash is common (petechiae may be seen on trunk, lower extremities, and mucous membranes - won’t blanch of fade under pressure).

Complications-
(Neck) - increased ICP: major cause of altered mental status

Brudzinski’s Neck Sign

(most common acute complication) - residual neurologic dysfunction: cranial nerves III, IV, VI, VII, or VIII can become dysfunctional.

— sequelae varies by cranial nerve (long term effects)
- hemiparesis, dysphagia and hemianopsia (loss of vision in one of the visual fields)
- suspect the following if hemiparesis, dysphagia and hemianopsia doesn’t resolve: cerebral abscess, subdural empyema, subdural effusion or persistent meningitis.
Acute cerebral edema may cause: seizures, CN III palsy, bradycardia, hypertensive coma, death
- waterhouse friderichsen syndrome: is a complication of meningococcal meningitis. Is manifested by petechiae, DIC, adrenal hemorrhage and circulatory collapse

DX studies: blood culture, CT scan, neutrophils are predominant in WBC in CSF, x-ray of skull, MRI
DX verified: lumbar puncture (once CT rules out obstruction - decreased glucose and increased protein = bacterial meningitis), analysis of CSF, specimens of secretions are cultured ( CSF, Sputum, nasopharyngeal

secretions) to identify causative organisms, gram-stain to detect bacterial

Interprofessional care: - medical emergency
- rapid dx is crucial

— the patient is usually critical when health care is initiated — antibiotic therapy instituted before diagnosis is confirmed.

- corticosterioids (dexamethasone) before or with first dose of antibiotics.
- antibiotics commonly prescribed: ampicillin, penicillin, vancomycin, cefuroxime (Ceftin), cefotaxime

(claforan), ceftriaxone (rocephin), ceftzoxime (cefizox), and ceftazidime (ceptaz)

Nursing implementation:
- vaccinations for pneumonia and influenza
- meningococcal vaccines
- early treatment of respiratory tract and ear infections
- PROPHYLACTIC ANTIBIOTICS FOR ANYONE EXPOSED.

-

Inflammatory Brain Disorders

Viral meningitis

- most common causes are enterovirus, arbovirus, HIV and HSV
- most often spread thru direct contact with respiratory secretions.

- usually presents as a headache, fever, photophobia and stiff neck
- is often self-limiting and patients have full recovery
Diagnostic testing: rapid dx with Xpert EV test (sample CSF is evaluated for enterovirus, results ready within hours)

PCR to detect viral specific DNA/RNA
Treat with antibiotics after obtaining dx sample but before receiving test results

Encephalitis

- acute inflammation of the brain
- serious and sometimes fatal disease

- caused by a number of viruses (some are endemic to specific geographic areas / seasons) - ticks or mosquitoes can transmit epidemic encephalitis
- cytomegalo virus (CMV) encephalitis s common with AIDS.
- HSV encephalitis is most common cause of acute non-epidemic viral encephalitis

Non specific onset: fever, headache, nausea, vomiting.
Signs appear in 2-3 days: may vary from minima alterations in mental status to coma but any CNS abnormality can occur

West nile is suspected if >50 years old and during summer or fall.

Nursing management:
- acyclovir (zovirax), vidarabine (vira-A) for encephalitis from HSV infection

- reduce mortality rates
- may not reduce neuro complications - start treatment before onset of coma

- anti seizure drugs
- may be initiated prophylactically in severe cases.

Head injury

Overview TBI

- any trauma to the skull, scalp or brain, TBI
- the most common causes: falls, MVAs
- other causes: firearm related injuries, assaults, sports related injuries, recreational injuries, war related injuries

- 2x as common in males

(Traumatic brain injury)

Scalp Lacerations

1-

- high potential for poor outcome
- deaths occur at 3 pointes in time after injury

(1) immediately after the injury (massive shock / hemorrhage)
(2) within 2 hours after the injury (brain injury / internal bleeding) (3) 3 weeks after the injury (multisystem organ failure)

- external head trauma
- scalp is highly vascular —> profuse bleeding - major complications: blood loss and infection

- linear (when there is a break in continuity of bone without alteration of relationship of parts. Is associated with low-velocity injuries) or depressed (is an inward indentation of skull and is associated with a powerful blow)

- simple (without fragmentation or communicating lacerations. Is caused by low to moderate impact), comminuted (occurs when there are multiple linear fractures with fragmentation of bone into many pieces. It is associated with direct / high momentum impact), compound (is a depressed skull fracture and scalp laceration with communicating pathway to intracranial cavity, is associated with severe head injury)

- closed or open (depending on the presence of scalp laceration or extension of the fracture into the air sinuses or dura),

- location determines manifestations
- complications: infections, hematoma, tissue damage
- in cases where basilar skull fracture is suspected — an orogastric tube should be used rather than an NG tube.

Skull fractures

Types of head injuries

- diffuse (generalized) — change of LOC —> minor concussion, diffuse axonal - concussion (sudden transient head injury)

- brief disruption in LOC, retrograde amnesia, headache, short duration (5 mins or less), may result in post concussion syndrome

- focal (localized) —> contusion or hematoma - minor (GCS: 13 - 15)
- moderate (GCS: 9 - 12)
- severe (GCS: 3 - 8)

Head injury

T- A basilar skull fracture is a specialized type of linear fracture that occurs when the fracture involves the base of

Raccoon Eyes & Battle Sign

the skull.
- Manifestations can evolve over the course of several hours, vary with the location and severity of fracture, and may include cranial nerve deficits

- Battle’s sign (postauricular ecchymosis)

- periorbital ecchymosis (raccoon eyes).
- This fracture generally is associated with a tear in the dura and subsequent leakage of CSF.

- Rhinorrhea (CSF leakage from the nose) or otorrhea (CSF leakage from the ear) generally confirms that the fracture has traversed the dura.

- Rhinorrhea may also manifest as postnasal sinus drainage.
- The significance of rhinorrhea may be overlooked unless the patient is specifically assessed for this

finding.
- The risk of meningitis is high with a CSF leak, and antibiotics should be administered to prevent the

development of meningitis.
- Two methods of testing can be used to determine whether the fluid leaking from the nose or ear is CSF.

- The first method is to test the leaking fluid with a Dextrostix or Tes-Tape strip to determine whether glucose is present. CSF gives a positive reading for glucose.

- If blood is present in the fluid, testing for the presence of glucose is unreliable because blood also contains glucose.

- In this event, look for the halo or ring sign. To perform this test, allow the leaking fluid to drip onto a white gauze pad (4 × 4) or towel, and then observe the drainage. Within a few minutes, the blood coalesces into the center, and a yellowish ring encircles the blood if CSF is present.

— Note the color, appearance, and amount of leaking fluid because both tests can give false-positive results.

Nursing assessment

Subjective data-
- health perception management

1-

- alcohol / drug use (risk taking behaviors) Cognitive perception

- headache
- mood or behavioral changes
- mentation changes / impaired judgement - aphasia / dysphasia

Coping stress tolerance
- fear, denial, anger, aggression, depression

Objective data-
- rhinorrhea, impaired gag reflex, altered / irregular respirations - cushing’s triad: impending herniation) — cardiovascular

Head injury

-

Intracranial pressure

Interprofessional care

Drug therapy (to decrease ICP)
- mannitol (Osmitrol) — moves fluid from tissue to the vessels.

- plasma expansion
- osmotic effect
- monitor fluid and electrolyte status

- hypertonic saline (3%)
- moves water out of cells and into the blood - monitor BP and serium sodium levels

- normal ranges for sodium: 135-145 - if effective ICP will decrease

- corticosteroids
- dexamethasone (Decadron)
- vasogenic edema - surrounding tumor./ abscess
- monitor fluid intake, serum sodium (135 - 145), and glucose levels
- concurrent antacids, H2 receptor blockers, PPI (protonix)
- complications: hyperglycemia, increased risk of infection, GI bleeding.

- anti seizure drugs
- antipyretics ( acetaminophen)
- sedatives
- analgesics
- barbituates: pentobarbital (Nembutal) / thipental (pentothal)

- decrease ICP, decrease cerebral edema, decrease cerebral metabolism

Light sedation-
- midalzolam (versed - lorazepam (ativan)

Intracranial pressure

Nutritional therapy

Nursing assessment

F- hypermetabolic and hypercatabolic state increases need for glucose - enteral / parenteral nutrition
- early feeding (within 3 days of injury)
- keep patient normovolemic

- IV 0.9% NaCl preferred over D5W or 0.45 % NaCl - NaCl or D5w can increase cerebral edema

Cranial nerves
- eye movement: CN III, IV, VI
- corneal reflex: CN V, and VII
- oculocephalic reflex (doll’s eyes)

- to test turn head briskly while holding eyelids open - oculovestibular (caloric stimulation)

(Bad)

-

Amyotrophic Lateral sclerosis ( ALS)

ALS
(Lou gerig’s disease)

- a rare progressive neurologic disorder characterized by loss of motor neurons
- motor neurons in the brainstem and spinal cord generally degenerate —> progressive muscle weakness - electrical and chemical message originated in the brain don’t reach the muscles to activate them
- death respiratory infection
- no cure: general death within 2 to 5 years of dx.
- Riluzole (Rilutek), Edaravone (Radicava), medications that slow progression
- patient remains cognitively intact while wasting away

Signs & symptoms

- tripping, dropping things, muscle cramps and twitching, spasticity, hyperreflexia (increased response to reflexes) - weakness of the upper extremities
- dysarthria (slurred speech)
- dysphagia, drooling, esophageal reflux

- pain
- sleep disorders
- emotional disorders
- constipation
- muscle atrophy
- progressive muscle weakness

Nursing interventions

- support patients cognitive and emotional functions - facilitate communication
- reduce risk of aspiration
- decrease pain

- decrease risk of injury
- provide diversional activities
- anticipatory grieving
- discuss advanced directives (have ahead of time) - voice banking

-

Guillain Barre Syndrome

IANS dysfunction Cranial nerve involvement

Complications

Collaborative care

- orthostatic hypotension
- hypertension, abnormal vagus response bradycardia, heart block, asystole (flat line) - bowel and bladder dysfunction
- facial flushing
- diaphoresis
- SIADH

- facial weakness, eye movement difficulties - dysphagia, paresthesia of the face

RESPIRATORY FAILURE

- constant monitory of respiratory system
- urinary tract infections
- immobility- paralytic ileus, muscle atrophy, DVT, PE, skin breakdown, orthostatic, hypotension, nutritional

deficiencies

- ventilatory support
- plasmapheresis
- IV high dose immunoglobulin (IG ig) - corticosteroids (unsure of effect)
- nutritional therapy

Nursing management

- Assessment
- ascending paralysis (from the ground up)
- sensation isn't lost, may be hypersensitive to pain and touch - respiratory function
- VS

Motor: what they can move / their strength Sensory: what they feel

Diabetes Insipidus

Diabetes Insipidus

Caused by:
- a deficiency of production or secretion of ADH
- a decreased renal response to ADH
Results in:
- F&E imbalance that is caused by: increased urinary output and increased plasma osmolality - transient or lifelong

Types / classifications

- neurogenic (central)
- nephrogenic (vasopressin resistant) - dispogenic (primary)
- gestagenic (gestational)

Neurogenic (central)

- most common form
- results of interference with ADH (vasopressin) synthesis, transport or release
- examples: brain tumor, head injury, brain surgery, CNS (central nervous system) infections
Treatment:
- desmopressin (DDAVP) synthetic Vasopressin (replacement choice)
- pitressin
- chlorpropamide (Diabinase) or carbamazepine (tegratol) to decrease thirst (may act to increased ADH release or

enhance the effects of ADH on the renal tubules)

Nephrogenic (Vasopressin resistant)

- results from inadequate renal response to ADH
- examples: drug therapy (lithium), renal damage, hereditary renal disease

Dispogenic (primary)

- results from excessive water intake (abnormal thirst)
- examples: structural lesion in the thirst center, psychological d/o

Gestagenic (Gestational)

- result of deficiency of ADH (vasopressin) that occurs only during pregnancy

Clinical manifestations of diabetes insipidus

- polydipsia: excessive thirst
- polyuria: excessive urine
- 2 to 20 L/urine per day (normal is 30cc / hour)
- low specific gravity (SG) less than 1,005 - low urine osmolality
- elevated serum osmolality
- weight loss, constipation, poor tissue turgor, low BP, high HR, shock - CNS manifestations

Diagnostic studies

- water deprivation tests confirms diagnosis by demonstrating renal inability to concentrate urine - Urinalysis: colorless urine, low osmolality, low specific gravity

Collaborative care

- determine and treat the primary cause - goal is to maintain F&E balance
- hypotonic saline - in neurogenic

- diuretics: in nephrogenic DI
- diet therapy: in nephrgenic DI

- man made form of vasopressin (DDAVP, Pitressin) in neurogenic

Diabetes Insipidus

Nursing management

- early detection
- maintain adequate hydration - daily weights
- vital signs
- labs

l - changes in level of consciousness (LOC)
- patient teaching for long-term management

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

SIADH

- occurs when ADH is released despite normal or low plasma osmolarity
- abnormal production or sustained secretion of ADH
- excessive amount of serum ADH resulting in water intoxication and hyponatremia (a condition that

occurs when the level of sodium in the blood is too low. Normal sodium range: 135 - 145)

Characterized by

- fluid retention
- serum hypo-osmolality - dilutional hyponatremia

(sodium less than 135: normal range: 135 - 145)
- hypochloremia (normal chloride levels: 96 - 106)
- concentrated urine with increased or normal intravascular

volume
- normal renal function

Clinical manifestations

- headache, fatigue, anorexia, nausea, muscle aches
- abdominal cramps, weight gain without edema
- altered LOC, seizures, coma, small amounts of concentrated amber colored urine

Causes

- malignant tumors *small (oat) cell lung, pancreas, lymphoid cancers
- CNS disorders, head injury, CVA
- drug therapy
- miscellaneous conditions: positive pressure ventilation, trauma, pain, stress, acute psychosis

Diagnostic studies

- simultaneous measurement of urine and serum osmolality
- serum osmolality much lower than the urine osmolality indicates the inappropriate excretion of concentrated urine in

the presence of dilute serum
- decreased BUN (normal range: 6 - 24), Cr clearance (normal range: 77-160), Hgb (men 13.2-16.6 / women

11.6-15), and Hct (men: 38.3-48.6% / women: 35.5 - 44.9 %)

Collaborative care

- avoid or discontinue medications that stimulate the release of ADH - fluid restriction (some cases 3% NaCl)
- diuretic
- declomycin

Nursing management

- low urine output high specific gravity - sudden weight gain
- serum sodium decline
- restrict fluid intake

- position
- protect from injury - seizure precautions

- HOB positioning
- frequent positioning / turning
- frequent oral hygiene
- distractions to decrease discomfort of thirst

Burns

Types

- thermal burns - electrical burns
- chemical burns - cold thermal injuries - smoke inhalation injury

Thermal burns

- caused by flame, flash, scald (can occur in the bathroom or when cooking), or contact with hot objects - most common type of burn injury
- severity of injury depends on: temperature of burning agent / duration of contact time

Chemical burns

- results of contact with acids, alkalis and organic compounds
- alkali burns are hard to manage because they cause protein hydrolysis and liquefaction

- damage continues after alkali is neutralized
- alkali adheres to tissue
- alkali are found in cement, oven and drain cleaners, as well as industrial cleansers

- results in injuries to: skin, eyes, respiratory system, liver and kidney
- chemicals should be quickly removed from the skin, clothing containing chemical should be removed - tissue destruction may continue up to 72 hours after chemical injury.

Smoke inhalation injuries

- from inhalation of hot air or noxious chemicals - cause damage to respiratory tract
- major predictor of mortality in burn victims
- need to be treated quickly

- assess signs and symptoms of airway compromise and pulmonary edema can develop over the first 12 - 48 hours - 3 types

- metabolic asphyxiation
- carbon dioxide (CO) poisoning
- CO is produced by incomplete combustion of burning materials
- inhaled CO displaces oxygen —> hypoxia, carboxyhemoglobinemia, death

- hypoxia and ultimately death when CO levels are 20% or greater - treat with 100% humidified oxygen
- may occur in the absence of burn injury to the skin

- upper airway injury
- injury to the mouth, oropharynx and / or larynx

- manifested by: redness, blistering and edema
- caused by thermal burns or inhalation of hot air, steam, or smoke - swelling may be massive / and onset rapid

- eschar and edema may compromise breathing, swelling from scald burns can be lethal - mechanical obstruction can occur quickly —> true airway emergency

- lower airway injury
- injury to trachea, bronchioles and alveoli
- injury is related to length of exposure to smoke or toxic fumes - pulmonary edema may not appear until 12-48 hours after burn

- manifests as ARDs

Burns

Location of burn classification

- severity of burn injury is determined by location of the burn wound
- face, neck, chest —> respiratory obstruction
- hands, feet, joints, eyes —> self care troubles
- ears, nose, buttocks, perineum —> infection risk due to the underlying skeleton frequently being

exposed
- circumferential burns of extremities can cause circulation problems distal to the burn
- patients may also develop compartment syndrome from direct heat damage to the muscle and subsequent

edema / pre-burn vascular problems

Risk factors

- pre existing heart, lung, and kidney disease contribute to poorer prognosis
- diabetes mellitus and peripheral vascular disease contribute to poor healing and gangrene - physical weakness renders patient less able to recover

- alcoholism, drug abuse, malnutrition
- concurrent fractures, head injuries and other trauma leads to more difficult time recovering

Pre hospital care

Electrical injuries: remove the patient from the contact source
Chemical injuries: treat quickly by removing solid particles, use water lavage

- tissue destruction may continue up to 72 hours after a chemical burn. Small thermal burns: cover with clean, cool, tap water - damp towel
Large thermal burns: airway, breathing, circulation (ABCs)

- cool burns for no more than 10 minutes
- don’t immerse in cool water or pack with ice - remove burned clothing
- wrap in clean, dry sheet or blanket

Prehospital phase

- inhalation injury
- watch for signs of respiratory distress
- treat quickly and efficiently
- 100% humidified oxygen if CO poisoning is suspected

Emergent phase

- emergent (resuscitative) phase is time required to resolve immediate problems resulting from injury - up to 72 hours
- primary concerns: hypovolemic shock (not enough fluid), edema

-fluid and electrolyte shifts (greatest threat is hypovolemic shock)
- caused by a massive shift of fluids out of blood vessels as a result of increased capillary

permeability
- can begin as early as 20 minutes post burn
- colloidal osmotic pressure decreases
- more fluid shifting out of vascular space into interstitial spaces
—> “third spacing” when fluid moves to an area that has minimal to no fluid —> normal insensible loss: 30 to 50 mL/hr
—> severely burned patient: 200 to 400 mL/hr

Burns

Emergent phase - continued

- fluid and electrolyte shifts
- RBCs are hemolyzed by a circulating factor released at time of burn - thrombosis
- elevated hematocrit (normal range: 38.5 - 50)

- usually caused by: hemoconcentration due to fluid loss
- K+ shift develops first because injured cells and hemolyzed RBCs release K+ into the

extracellular space - inflammation and healing

- neutrophils and monocytes accumulate at site of injury

- fibroblasts and collagen fibrils begin wound repair within the first 6 to 12 hours after injury - immunologic changes

- immune system is challenged when burn injury occurs
- skin barrier is destroyed
- bone marrow is depressed
- circulating levels of immune globulins are decreased - WBCs develop defects

Clinical Manifestations: shock from hypovolemia, blisters, paralytic ileus (larger burn), shivering (result of chilling), altered mental status
- other possible: head trauma, hx of substance abuse, excessive pain / sedation meds.
- partial thickness burns commonly have blisters filled with fluid and protein

- full thickness & partial thickness burns are often painless due to destroyed nerve endings.

Complications: dysrhythmias and hypovolemic shock, impaired circulation to extremities
—> if left untreated: tissue ischemia, paresthesia, necrosis
- circulation to extremities can be severely impaired by deep circumfernetial burns and subsequent

edema formation which acts like a tourniquet Cardiovascular complications:

- impaired microcirculation and increased viscosity —> sludging (corrected by adequate fluid replacement)

- VTE —> more common if: advanced age, morbid obese, prolonged immobility, extensive lower extremity burns, concomitant lower extremity trauma

Respiratory complications:
- upper airway burns: edema formation, mechanical airway obstruction and asphyxia
- lower airway burns
—> may need a fiberoptic bronchoscopy and carboxyhemoglobin blood level to confirm smoke inhalation - pneumonia (common complication)
- pulmonary edema (leading cause of death in patients with inhalation injury)

Burns

Emergent phase- interprofessional management

- fluid replacement takes priority over nutritional needs
- early / aggressive nutritional support within hours of burn injury

- decreases complications and mortality - optimizes burn wound healing
- minimizes negative effects

- nutritional therapy
- hypermetabolic state

- resting metabolic expenditure may be increased by 50-100% above normal - core temp. Is elevated
- caloric needs are about 5,000 kcal/day

Acute phase

- begins with mobilization of extracellular fluid and subsequent diuresis
- concludes when: partial thickness wounds are healed and/or full thickness burns are covered by skin grafts

Patho:

- necrotic tissue begins to slough
- granulation tissue forms
- partial thickness burn wounds heal from edges and from dermal bed
- full thickness burns must have eschar removed and skin grafts applied

Clinical manifestations:
- partial thickness wounds form eschar — once eschar is removed, reepithelialization begins - full thickness wounds require debridement

Complications:

- infection
- localized inflammation, induration and suppuration
- partial thickness burns can change to full thickness wounds in the presence of infection
- watch for S&S: hypothermia / hyperthermia, increased HR / RR, decreased BP, decreased urinary output

- musculoskeletal system
- decreased ROM and contractures

- GI system
- paralytic ileus, diarrhea, constipation, curling’s ulcers

- endocrine system
- increased blood glucose levels, increased insulin production, hyperglycemia

Wound care:

- appropriate coverage of graft - grafts are left open

- complication: blebs (serosanguineous exudate), prevent the graft from permanently attaching the wound bed

Burns

Rehab phase

- begins when ' the wounds have healed and the patient is engaging in some level of self-care - can occur as early as 2 weeks or as long as 7 to 8 months after a major burn

- in approximately 4 to 6 weeks the are becomes raised and hyperemic - mature healing is reached about 12 months
- skin never completely regains its original color

- discoloration of scar fades with time
- newly healed areas can be hypersensitive or hyposensitive to heat / cold / touch - scarring has 2 components:

(1) discoloration / (2) contour

Complications:
- skin / joint contractures (most common during this phase)

- are a result of shortening of scar tissue in the flexor tissue of a joint
- positioning, splinting and exercise should be used to minimize contractures