Multi-System Trauma Pt. 2 (Head Injury and Burns) Flashcards
Skull has what 3 essential components?
Brain tissue
Blood
Cerebrospinal fluid (CSF)
enclosed space - rigid vault
The intracellular and extracellular fluids of brain tissue make up approximately ___% of this volume
78
Blood in the arterial, venous, and capillary network makes up ____% of the volume
12
____% is the volume of the CSF.
10
Primary injuryoccurs at the
initial time of an injury (e.g., impact of car accident, blunt-force trauma) that results in displacement, bruising, or damage to any of the three components.
- injury on impact
Secondary injuryis the resulting
hypoxia, ischemia, hypotension, edema, or increased ICP that follows the primary injury.
- after injury (swelling, hypoxia, HTN)
Secondary injury, which could occur several
hours to days after the initial injury, is a primary concern when managing brain injury
cerebral edema
increased accumulation of fluid in the extravascular spaces of brain tissue
cerebral edema results in an
increase in tissue volume that can increase ICP
Intracranial pressure (ICP)is the
hydrostatic force measured in the brain CSF compartment
What maintains the ICP?
the balance among the three components (brain tissue, blood, CSF)
Factors that influence ICP under normal circumstances are changes in
(1) arterial pressure; (2) venous pressure; (3) intraabdominal and intrathoracic pressure; (4) posture; (5) temperature; and(6) blood gases, particularly CO2levels.
The Monro-Kellie doctrine states that the
three components must remain at a relatively constant volume within the closed skull structure
- displaced, the total intracranial volume will not change.
-This hypothesis is only applicable in situations in which the skull is closed. The hypothesis is not valid in persons with displaced skull fractures or hemicraniectomy.
ICP can be measured in the
ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer
Normal ICP ranges from
5 to 15 mm Hg. *
A sustained pressure greater than 20 mm Hg is
considered abnormal and must be treated.*
What component is the first to go down when increased ICP?
CSF - swelling and edema
What goes down next after CSF goes down?
Blood
because it can not circulate – hypoxia and ischemia
Brain tissue with increased ICP
atrophy, herniation of the foramen in the brain stem
Herniation
poor prognosis
Cerebral blood flow(CBF) is the **
amount of blood in milliliters passing through 100 g of brain tissue in 1 minute**.
The maintenance of blood flow to the brain is critical because the
brain requires a constant supply of O2and glucose
brain uses ___% of the body’s O2and 25% of its glucose
20
Autoregulationis the
automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow during changes in arterial blood pressure (BP).
purpose of autoregulation is to ensure a
consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits
- consistent blood to the brain
- will add or remove O2 when needed by vasodilation or vasoconstriction
CBF decreases, and symptoms of cerebral ischemia, such as
syncope and blurred vision
High CBF can be affected by
(>150 MAP)
cardiac or respiratory arrest, systemic hemorrhage, and other pathophysiologic states (e.g., diabetic coma, encephalopathies, infections, toxicities
Regional CBF can be affected by
trauma, tumors, cerebral hemorrhage, or stroke. – lose elasticity (tx with shunt to get fluid out)
CPP =
MAP - ICP
CPP
force driving blood into the brain, providing oxygen and nutrients
- ensure blood flow to the brain
ICP increased by
intracranial bleeding
cerebral edema
tumor
Increased ICP causes
collapsed veins
decrease effective CPP
reduces blood flow
primary determinant ofcerebral blood flow
CPP
Normal CPP is
60 to 100 mm Hg
CPP decreases
autoregulation fails and CBF decreases
CPP of less than 50 mm Hg is associated with
ischemia and neuronal death.
A CPP of less than 30 mm Hg results in
ischemia and is incompatible with life.
Increased ICP S/S
change in LOC
HA, vomiting w/ no N
change in speech
Papilledema
Pupillary changes
impaired eye mvmt
Posturing
flaccid
low motor function
seizures
Cushing’s Triad
- no fever or loss of smell
Cushing’s Triad
high systolic BP
low HR
altered respiratory pattern (Kussmaul’s, Cheyne-stokes
major complications of uncontrolled increased ICP are
inadequate cerebral perfusion and cerebral herniation
Increased ICP mgmt
HOB 30
Head midline with towel rolls
Low stimulation environment
Cluster care
Help family understand (hearing is the last to lose)
- Keep calm and let them rest
Cushing’s Triad is a __________ emergency
neurological
-ominous development
-rapid fluctuations of VS
brain compression s/s
increases, respirations become rapid, the blood pressure may decrease, and the pulse slows further
Pressure-Volume Curve
stage 1
high compliance
The brain is in total compensation, with accommodation and autoregulation intact. An increase in volume (brain tissue, blood, or CSF) does not increase the ICP.
Pressure-Volume Curve
stage 2
compliance is beginning to decrease, and an increase in volume places the patient at risk of increased ICP and secondary injury.
Pressure-Volume Curve
stage 3
significant reduction in compliance. Any small addition of volume causes a great increase in ICP. Compensatory mechanisms fail, there is a loss of autoregulation, and the patient exhibits manifestations of increased ICP (e.g., headache, changes in level of consciousness or pupil responsiveness).
With a loss of autoregulation, the body attempts to maintain cerebral perfusion by increasing systolic BP.
- decompensation is imminent.
- systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations.
Pressure-Volume Curve
stage 4
ICP rises to lethal levels with little increase in volume
-herniation
Herniation
occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a compartment of lesser pressure. In this situation, intense pressure is placed on the brainstem, and if herniation continues, brainstem death is imminent.
ICP should be monitored in patients admitted with a
Glasgow Coma Scale (GCS) score of 8 or less and an abnormal CT scan or MRI
Monitoring ICP types
Subdural
Epidural
Subarachnoid
Intraparenchymal
Ventricular- gold standard
Monitoring ICP mgmt
labs and VS for infection (hot, flush, and running a fever)
Sterility
Do not change
Central lines
Biopatch
ICP tubing mgmt for nursing
Medications in tubing are only by the physician
Mark it off with labels
Watch temp.
Keep control of the tubing and tidy
Monitor and trend
Good oxygenation and in normal ranges with ABG
Interprofessional CARE for ICP
Identify and treat the underlying cause
Support brain function
- O2, ETT/VENT, ABG
Drug therapy
Nutritional therapy
The underlying cause of increased ICP is usually an
increase in blood (hemorrhage), brain tissue (tumor or edema), or CSF (hydrocephalus) in the brain.
- BE THERE TO SIMPLIFY THE NEUROSURGEON’S WORDS
What is the best tx for increased ICP caused by a mass lesion
surgical removal of the mass
Head trauma includes an
alteration in consciousness, no matter how brief
Deaths occur at what three points in time after injury
Immediately after the injury
Within 2 hours after injury
3 Weeks after injury – septic infection
Highest risk for head injury
15-24 y/o
males
<5 and >75
Primary injury is the
initial damage to the brain that results from the traumatic event. This may include contusions, lacerations, and torn blood vessels due to impact, acceleration/deceleration, or foreign object penetration.
Secondary injury evolves
evolves over the ensuing hours and days after the initial injury and results from inadequate delivery of nutrients and oxygen to the cells
Scalp lacerations
easily recognized type of external head trauma
-excessive bleeding
main concern is blood loss and infection
Skull Fx types
occur with head trauma
(1) linear or depressed; (2) simple, comminuted, or compound; and
(3) closed or open
open fx is anything
exposed around the site of injury
- give antibiotics
Diffuse Injury
Concussion
Diffuse axonal injury DIA
Focal Injury
Lacerations
Contusion - bruise
Coup-Contrecoup – shaken baby syndrome
minor head injury GCS
13-15
moderate head injury GCS
9-12
severe head injury GCS
3-8
Concussion
a sudden transient mechanical head injury** with disruption of neural activity and a change in the LOC
-minor diffuse
S/S of concussion
brief disruption in LOC, amnesia regarding the event (retrograde amnesia), and headache
Get worst the more they get (boxers and football players with speech)
No contact sports is recommended at elementary to junior high
DAI
widespread axonal damage occurring after a mild, moderate, or severe TBI. The damage occurs primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus, and brainstem
Basilar Fx
base of the skull
- CSF leakage (HALO and glucose dipstick+)
- dura tear
- major infection
Complication of Head Injury
Hematomas
Hemorrhages
Epidural hematoma location
bleeding between the dura and inner surface of the skull
Epidural hematoma associated with
neurologic emergency and is usually associated with a linear fracture crossing a major artery in the dura, causing a tear
Acute subdural hematoma type
compression with increase ICP
24-48 hours
Acute subdural hematoma s/s
HA
vomiting
Epidural hematoma bleed from
middle meningeal artery (medical emergency)
Considered the Walking dead
Epidural hematoma classic s/s
initial period of unconsciousness at the scene, with a brief lucid interval followed by a decrease in LOC
- HA, N/V
Acute subdural hematoma bleed from
Venous blood – slower
**Bridging veins
- Not right away to the OR wait for them to seal on themselves
subacute subdural hematoma
2nd CT notice more bleeding
- appear to enlarge over time
Tx needed
s/s increase ICP
- 2-14 days
chronic subdural hematoma
Age shrinks the brain
More room in head
Without s/s and they have a bleed
Falling risk elderly
Alcoholics: multiple falling incidence bc they don’t remember the night of falling
weeks to months
subdural hematomaoccurs from bleeding
between the dura mater and arachnoid layer of the meninges
Intracerebral Hemorrhage where
Occurs from bleeding within the parenchyma
Usually occurs in the frontal and temporal lobes
Size and location determine patient outcome
Subarachnoid Hemorrhage where
Bleeding into the subarachnoid space
What mimics a severe migraine
subarachnoid hemorrhage
Intracerebral Hemorrhage onset
insidious, beginning with the development of neurologic deficits followed by headache
Intracerebral Hemorrhage mgmt
supportive care, control of ICP, and careful administration of fluids, electrolytes, and antihypertensive medications
Intracerebral Hemorrhage surgical intervention
craniotomy or craniectomy permits removal of the blood clot and control of hemorrhage but may not be possible because of the inaccessible location of the bleeding or the lack of a clearly circumscribed area of blood that can be
Intracerebral Hemorrhage Tx
Tx the s/s and wait for the blood to be reabsorbed
Diffuse axonial bleed
Subarachnoid Hemorrhage results after
result of an AVM, intracranial aneurysm, trauma, or hypertension. The most common causes are a leaking aneurysm in the area of the circle of Willis and a congenital AVM of the brain
Vasospasm
narrowing of the lumen of the involved cranial blood vessel
Vasospasm monitoring
transcranial Doppler ultrasonography (TCD) or follow-up cerebral angiography
Vasospasm occurs
3 to 14 days after initial hemorrhage, when the clot undergoes lysis (dissolution), and the chance of rebleeding is increased
Vasospasm leads to
increased vascular resistance, which impedes cerebral blood flow and causes brain ischemia and infarction
Brain Hemorrhage c/o
severe migraine, HA, thunderclap
photophobia, N/V
Similar to a migraine incident and need to be seen by physician to determine the difference
Cause of Brain Hemorrhage
berry aneurysm in the bifurcation (trauma, uncontrol HTN)
irritates of the vessel until weakening
3-14 days after
Tx of vasospasm
hypovolemic give fluids, permissively HTN, Nimotop(beta blocker/Ca blocker with regularity and on time)
UNTx of vasospasm
hypoxia = ischemia= cell death
Nursing Mgmt for Brain Hemorrhage
Airway - HOB 30, suctioning, O2, ABG, prevent mech vent complications
Glasgow Coma Scale score
VS - Cushing’s, T<100.4, high HR, arterial low BP
Neurologic status frequently
Presence of CSF leak
Brain Hemorrhage major s/s
A,Raccoon eyes and rhinorrhea.
B,Battle’s sign (postauricular ecchymosis) with otorrhea.
C,Battle’s sign.
D,Halo or ring sign
Rhinorrhea
CSF leakage from the nose
- postnasal sinus drainage
otorrhea
CSF leakage from the ear
What complications need to be assessed and prevented with CSF leakage?
meningitis - antibiotics
CSF leakage determining
Dextrostix or Tes-Tape strip
+ glucose
HALO sign
If the drainage is annoying, then what can the nurse do?
white gauze pad (4 × 4) or towel, and then observe the drainage.
- Do not pack the area of leakage – gauze under the ear to catch and collect (prevent trapping it in an infected area
major potential complications of skull fractures
are intracranial infections, hematoma, and meningeal and brain tissue damage
CSF looks like
straw color, sweet, sticky
Basilar Fx should not have
NG Tubes – risks meningitis
GCS range
3-15
< 8 intubate
gold standard assessment tool for LOC
GCS
GCS baseline is
the best the person can do
- when to take off sedation need HCP orders
Nursing Acute Mgmt for head injuries
Maintain cerebral perfusion*
Prevent secondary cerebral ischemia*
Monitor for changes in neurologic status
Treatment of life-threatening conditions will initially take priority in nursing care*
- osmotic diuretics, SIADH, DI = electrolyte monitoring
- balance Na and glucose
Ambulatory and Home Care for Head Injuries
Nutrition, Bowel / bladder control
Seizure disorders, Personality changes
Family participation and education
- increase consumption of calorie and nitrogen excretion
protein demand
Pt Education Preventions for head Injuries
Advise all drivers and passengers to wear seat belts and shoulder harnesses
Caution passengers against riding in the back of pickup trucks
Promote educational programs directed toward violence and suicide prevention in the community
Teach patients steps to prevent falls, particularly in the elderly
Advise owners of firearms to keep them locked in a secure area where children cannot access them
Head Injuries affect what cranial nerves
1-3
Cranial Nerve 1 function
olfactory
Cranial Nerve 1 test
alcohol pad
Cranial Nerve 2 function
vision
Cranial Nerve 3 function
most eye muscles
Cranial Nerve 2 how to test
vision chart
Cranial Nerve 3
follow the finger
Types of Burns
Thermal
Chemical
Electrical
Smoke and inhalation
Cold thermal injury or frostbite
Thermal burns,caused by
flame, flash, scald, or contact with hot objects, are the most common type of burn injury. The severity of the injury depends on the temperature of the burning agent and duration of contact time. Scald injuries can occur in the bathroom or while cooking. Flash, flame, or contact burns can occur while cooking, smoking, burning leaves in the backyard, or using gasoline or hot oil.
Chemical burns
contact with acids, alkalis, and organic compounds. In addition to tissue damage, eyes can beinjured if they are splashed with the chemical. Acids are found in the home and at work and include hydrochloric, oxalic, and hydrofluoric acid. Alkali burns can be more difficult to manage than acid burns, since alkalis adhere to tissue, causing protein hydrolysis and liquefaction. Alkalis are found in cement, oven and drain cleaners, and heavy industrial cleansers.4Organic compounds, including phenols (chemical disinfectants) and petroleum products (creosote and gasoline), produce contact burns and systemic toxicity.
Electrical burns
intense heat generated from an electric current. Direct damage to nerves and vessels, causing tissue anoxia and death, can also occur. The severity of the electrical injury depends on the amount of voltage, tissue resistance, current pathways, surface area in contact with the current, and length of time that the current flow was sustained Tissue densities offer various amounts of resistance to electric current. For example, fat and bone offer the most resistance, whereas nerves and blood vessels offer the least resistance. Current that passes through vital organs (e.g., brain, heart, kidneys) produces more life-threatening sequelae than that which passes through other tissues. In addition, electric sparks may ignite the patient’s clothing, causing a flash injury.
- Take path of least resistance – skin and vessels to muscle and bone
Smoke and inhalation burns
noxious chemicals or hot air can cause damage to the respiratory tract. Three types of smoke and inhalation injuries can occur: metabolic asphyxiation, upper airway injury, and lower airway injury. Smoke inhalation injuries are a major predictor of mortality in burn patients. Rapid initial and ongoing assessment is critical. Airway compromise and pulmonary edema can develop over the first 12 to 48 hours.
Superficial Partial-Thickness
Should heal without intervention
Superficial
Epidermal layer
Pink to red
Uncomfortable to touch
Superficial Partial-Thickness s/s
Erythema, blanching on pressure, pain and mild swelling, no vesicles or blisters (although after 24 hr skin may blister and peel).
Superficial Partial-Thickness causes
cause-Superficial sunburn, Quick heat flash**
Superficial Partial-Thickness structure involved
Involved-Superficial epidermal damage with hyperemia. Tactile and pain sensation intact
Deep Partial-Thickness
Epidermal and dermal layer involved
Red mottled pink edges, hair remains intact
Very painful
Takes 2-4 weeks to heal
Sensitive to touch, cold and warm air
Moderate to severe pain
Blisters
Deep Partial-Thickness skin destruction
Fluid-filled vesicles that are red, shiny, wet (if vesicles have ruptured). Severe pain caused by nerve injury. Mild to moderate edema.
Deep Partial-Thickness causes
Flame
Flash
Scald
Contact burns
Chemicals
Tar, cement
Electric current
Deep Partial-Thickness structures involved
Epidermis and dermis involved to varying depths. Skin elements, from which epithelial regeneration occurs, remain viable.
Full-Thickness Burns
Full dermal layer involved
White, dry, leather like texture
No nerve endings = no pain
Full-Thickness Burns skin destruction
Dry, waxy white, leathery, or hard skin. Visible thrombosed vessels. Insensitivity to pain because of nerve destruction. Possible involvement of muscles, tendons, and bones
Full-Thickness Burns cause
Flame
Scald
Chemical
Tar, cement
Electric current
Full-Thickness Burns structure involved
All skin elements and local nerve endings destroyed. Coagulation necrosis present. Surgical intervention required for healing
ED, burn arms with grease fire
Indicated, Nonessential, contraindication
Indicated – Ivs, analgesics, tetanus toxoid
Nonessential – O2, EKG,
Contraindicated – shower in the first 12 hours
Burn from chest up
Indicated, contractions
Indicated O2, 2 IVS, analgesics, possible intubation
Contra – cool room
Inhalation Injury s/s
Blisters, edema
Difficulty swallowing
Hoarseness
Stridor
Retractions
Total airway obstruction
Damage mucosa
soot
Metabolic Asphyxiation
primarily carbon monoxide (CO) or hydrogen cyanide. Oxygen delivery to or consumption by tissues is impaired. The result is hypoxia and, ultimately, death whencarboxyhemoglobin(i.e., hemoglobin combined with CO) blood levels are greater than 20%. CO and hydrogen cyanide poisoning may occur in the absence of burn injury to the skin.
Upper airway injury
swelling can be massive and the onset rapid. Flame burns to the neck and chest may make breathing more difficult because of the burn eschar, which becomes tight and constricting from the underlying edema. Swelling from scald burns to the face and neck can also be lethal, as can external pressure from edema pressing on the airway. Mechanical obstruction can occur quickly, presenting a true airway emergency.
Lower airway injury pulmonary edema occurs after
12-48 hours after the burn - ARDS
Do you wait for intubation with inhalation injuries?
no
Do not wait for intubation due to swelling
Burnt skin and mucosa become tight and lead to mechanical obstruction
Electrical Injury
Masked marauder – under the skin is a tunneling mess going through everything from path of least resistance but only appears as a tiny hole
- EKG for dysrhythmias, SEVERE METABOLIC ACIDOSIS, AND MYOGLOBINURIA
How to tell the extent and depth of burn injuries?
Rule of Nines, Lund-Browder, or the Berkow charts calculate the total body surface area (TBSA) burned
The Rule of Palms can be used for scattered burns
Explain the Rule of 9s
Head front = 4.5%
Head Back = 4.5%
Upper chest and lower chest
and same with the back = 9% each
each leg as a whole is 18%
each arm is 9%
Palmar Method explaned
The pt palm is 1%
-scattered burns
Referral Criteria for burn victims
1.Partial-thickness burns >10% of total body surface area (TBSA)
2.Burns that involve the face, hands, feet, genitalia, perineum, or major joints**
3.Third-degree burns in any age group**
4.Electrical burns, including lightning injury**
5.Chemical burns**
6.Inhalation injury**
7.Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality risk (e.g., heart or kidney disease, diabetes)
8.Any patients with burns and concomitant trauma (e.g., fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn center. The HCP will need to use his or her judgment, in consultation with the regional medical control plan and triage protocols.
9.Burn injury in children in hospitals without qualified personnel or equipment needed to care for them
10.Burn injury in patients who will require special social, emotional, or long-term rehabilitative intervention
Associated Trauma for Burn victims
Remember the ABCs of trauma
Burns and inhalation injury frequently mask other injuries
Fractures
Spinal cord injury
Other trauma
- fluid and electrolytes shift
- inflammation and healing
- immunity
Fluid and Electrolyte Patho for burns
Fluid and Electrolyte shift
Inflammation and Healing
Immunologic Changes
Decrease vascular volume – cap becomes permeable (interstitial)
Decreased cardiac output
Increase blood viscosity
Inflammation and Healing patho for burns
Burn injury to tissues and vessels causes coagulation necrosis. Neutrophils and monocytes accumulate at the site of injury. Fibroblasts and newly formed collagen fibrils appear and begin wound repair within the first 6to 12 hours after injury
immunity patho for burns
skin barrier to invading organisms is destroyed, bone marrow depression occurs, and circulating levels of immunoglobulins are decreased. Defects occur in the function of white blood cells (WBCs). The inflammatory cytokine cascade, triggered by tissue damage, impairs the function of lymphocytes, monocytes, and neutrophils. Thus the patient is at a greater risk for infection.
S/S of electrolyte and fluids
Na INSIDE THE CELL
K outside the cell
Albumin, Na and water into interstitial space
Emergent Phase mgmt
care mainly focuses on airway mgmt
fluid therapy - 2 IVlarge
wound care
emotional support for all
teaching
Protect the team before providing care
ABCs of trauma
Protect the airway
Fluid needs
Metabolic and electrolytes
Psychosocial needs of the patient and the staff
What burn victim is the first to be seen?
deep partial thickness
- prepare for intubation
- post-anesthesia
- full thickness with dressing change
What is the 1st thing needed in assessing a burn victim?
protect environment
Fluid Resuscitation for Burn Victims for the first 24 hours
[Weight in Kg] X [TBSA burned] X [4 mL]
divide by half = 1st 8 hours
divide by half that number = next 8-8 hours
double check in L
Using the Parkland formula, the nurse determines that a patient requires a total of 12 L of fluid in the first 24 hours post injury. How much of the total volume needs to be given within the first 8 hours?
A. 4,000 mL lactated Ringer’s
B. 6,000 mL lactated Ringer’s
C. 8,000 mL lactated Ringer’s
D. 10,000 mL lactated Ringer’s
B. 6,000 mL lactated Ringer’s
Fluid losses in burn victims
3rd spacing
blisters and exudates
edema
insensible loss 30-50mL/hr
Fluid Mgmt after first 8 hours
Light wt diuretic
Turn down fluid given
Fluid loss from breathing 30-50 mL
Intubation
Humdify warm air
Blister formation =fluid loss
Reparative Phase
Wound care
Nutritional support
Management of pain
Prevention of contractures
Wound management
Psychosocial issues
Use of topical antimicrobials
Early debridement
Early excision and grafting
Contractions = passive or active ROM with analgesics
Scrubbed with brush - debridement
Strict infection control practices (i.e., physical isolation in a private room, use of gowns and gloves during patient contact, and handwashing before and after each patient visit
Psych consult and antidepressants
Rehabilitation and Reconstruction Phase of Burn victims
On going skin needs
Activity needs
Self-concept and depression
Noncompliance with care
Rehabilitation and Reconstruction Phase occurs
7-8 months after
Reconstruction Phase goals
(1) work toward resuming a functional role in society and (2) rehabilitate from any functional and cosmetic postburn reconstructive surgery that may be necessary
Mature healing is reached in about
12 months when suppleness has returned, and the pink or red color has faded to a slightly lighter hue than the surrounding unburned tissue.
A patient who is admitted to a burn unit is hypovolemic. A new nurse asks an experienced nurse about the patient’s condition. Which response if made by the experienced nurse is most appropriate?
“Blood loss from burned tissue is the most likely cause of hypovolemia.”
“Third spacing of fluid into fluid-filled vesicles is usually the cause of hypovolemia.”
“The usual cause of hypovolemia is evaporation of fluid from denuded body surfaces.”
“Increased capillary permeability causes fluid shifts out of blood vessels and results in hypovolemia.”
“Increased capillary permeability causes fluid shifts out of blood vessels and results in hypovolemia.”
????????? - doule check
