11.1

Critical Care

Chapter 11

Critical Care

Introduction

Each battlefield ICU should have a dedicated intensive care

physician, due to the severity and lethality of blast and highvelocity wounds, and the need for ongoing resuscitation of

casualties requiring damage control.

Damage control is the initial control of hemorrhage and

contamination followed by intraperitoneal packing and rapid

closure, then resuscitation to normal physiology in the

intensive care unit and subsequent definitive re-exploration.

This places large logistic requirements on the ICU. This may

include rewarming, large-volume resuscitation, blood

products, vasoactive drugs, and mechanical ventilation.

The ICU physician should observe the following guidelines:

 Reexamine (possibly, retriage) the patient, using detailed

primary and secondary surveys, with attention to the “ABCs,”

potential life-threatening injuries, and other injuries missed

during the ER and OR phases of resuscitation (tertiary survey).

Trust no one’s examination before your own because the

patient’s condition may have changed, or prior examinations

may be inaccurate or incomplete.

 Provide necessary available monitoring of physiology, with

periodic assessment of pain control, level of consciousness,

and intake and output.

 Resuscitate from shock, using appropriate endpoints.

 Provide organ-specific support, as is done for CNS injury,

pulmonary failure, cardiovascular collapse, and renal

dysfunction.
11.2

Emergency War Surgery

 Ensure adequate pain control.

ο Use IV (not IM) narcotic agents in sufficient doses to

alleviate pain.

ο Patients on mechanical ventilation require both narcotics

(morphine, fentanyl) and sedatives (propofol, lorazepam,

midazolam).

 Prepare the patient for transport out of theater.

 Important caveats for the intensivist.

ο “Patients don’t often suddenly deteriorate; healthcare

providers suddenly notice!”

ο The organ system approach, in which each organ system

in turn is addressed in a mini-SOAP format, ensures that

each of the body’s physiologic systems is addressed in a

complete, comprehensive, and integral fashion.

ο The systemic inflammatory response (SIRS) is a common

metabolic sequela of severe injury, not always associated

with infection.

Fever or leukocytosis should prompt a thorough search for

infection. Antibiotic discipline must be enforced, saving these

medications for short-course prophylaxis, documented

infection, or empiric treatment of rapid deterioration due to

sepsis.

Resuscitation From Shock

Shock can be defined as an acute state of cardiovascular

insufficiency resulting in life-threatening global

hypoperfusion. Hemorrhagic shock is the most common form

of shock following major trauma. Therefore, initial efforts

should be directed toward correction of hypovolemia.

Hypoperfusion implies inadequate delivery of oxygen to the

body’s cells. Oxygen delivery is a function of cardiac

performance, arterial hemoglobin content, and arterial oxygen

saturation. All attempts to correct shock involve optimizing

these three variables.
11.3

Critical Care

 Shock resuscitation is approached in two phases, based on

endpoints of resuscitation:

ο In the first phase, resuscitate to a mean arterial pressure

of > 60 mm Hg, a urine output of 0.5 cc/kg/h (at least 30

ccs/h), and arterial oxygen saturation of > 92%.

ο Pursue endpoints aggressively to eliminate hypoperfusion,

ideally within 1 hour (see Chapter 7, Shock and

Resuscitation).

ο In the second phase, resuscitation is continued primarily

with fluid, to eliminate metabolic acidosis (restore lactate

to normal) within 24 hours.

ο The resuscitative fluid of choice is a warmed, balanced

crystalloid solution (normal saline or lactated Ringer’s)

and is preferable to colloid.

ο Rate of infusion for resuscitation should be 500 mL to 1,000

mL bolus over 15–20 minutes and repeated as necessary.

ο After 3 L of crystalloid, blood products should generally

follow at similar rates.

Vasopressor agents should only be considered for achieving

minimal acceptable blood pressure after fluid boluses and

confirmation of adequate intravascular volume.

ο Dopamine, norepinephrine, and phenylephrine are the

preferred vasoactive agents, starting in the lower dose range.

ο Dobutamine should only be considered for demonstrated

cardiac dysfunction, which may be seen in sepsis, the

elderly, or myocardial infarction (MI).

Specific Organ Systems

Traumatic Brain Injury/CNS

Transient hypoxemia or hypotension in the patient with

significant traumatic brain injury doubles the probability of

death or poor neurologic outcome. The goal of treatment is to

maintain cerebral perfusion pressure (CPP) and oxygenation.
11.4

Emergency War Surgery

 Identify potential intracranial surgical lesions for possible

emergent craniotomy.

 Prevent hypoxemia: Maintain O2 sat > 92%, PaO2 > 100, and

intubate for GCS < 8.

 Prevent hypotension.

ο Maintain SBP > 100 mm Hg, MAP > 80.

♦ MAP = DBP + 1⁄3 (SBP - DBP).

 Prevent, monitor, and treat intracranial hypertension.

ο Maintain intracranial pressure (ICP) = 5–15 mm Hg.

ο Maintain CPP = 70–90 mm Hg.

CPP = MAP – ICP

 Measures to treat intracranial hypertension include:

ο Elevation of head of bed 30° may be helpful.

ο Recognize that high levels of PEEP may raise ICP.

ο Control serum osmolarity.

♦ Normal saline is the preferred IV solution.

♦ Check serum sodium twice daily, and keep in the range

of 145–150 mEq/dL.

♦ IV mannitol (not in anuric patients), 0.25–1.0 g/kg,

every 6–8 hours to keep serum osmolarity optimal.

ο Control PaCO2.

Hypercarbia should always be prevented. Modest

therapeutic hyperventilation may be used (PaCO2 30–35 mm

Hg) for brief periods in the deteriorating patient.

♦ Beneficial effects of hyperventilation/hypocarbia must

be balanced: it reduces ICP through vasoconstriction,

but also reduces cerebral blood flow.

♦ Prophylactic hyperventilation should not be used.

ο Removal of cerebrospinal fluid by placement of an

intraventricular catheter.

ο Barbiturates have unproven benefit but may be considered

in extreme cases.

ο Craniotomy with bone and brain removal is a drastic,

lifesaving procedure of last resort in the moribund patient.

Steroids have no role in traumatic brain injury treatment.
11.5

Critical Care

ο Avoid hyperthermia, because this raises ICP.

 General Considerations.

ο Appropriate precautions should be taken (H2 blocker,

heparin, and oral care) to prevent development of stress

gastritis, deep venous thrombosis, and aspiration

pneumonitis.

ο If coagulopathy develops, use blood products as necessary

to correct an elevated prothrombin time.

ο Prevent and aggressively treat pain, agitation, shivering,

and fever to avoid increased cerebral metabolism and

oxygen consumption.

ο Hyperglycemia has an adverse effect on outcome and

should be monitored and treated aggressively to keep

glucose levels between 100–150 mg/dL.

ο Seizure prophylaxis. Phenytoin/phosphenytoin should be

administered to therapeutic levels in the penetrating headinjured patient, and to blunt head-injury patients with

seizure.

Pulmonary System and Ventilators

General Considerations

 Supplemental oxygen in the early phase of resuscitation is

imperative. The maximum fraction of inspired oxygen (FIO2)

delivered by:

ο Nasal cannula approaches 0.35.

ο Venturi mask is 0.50.

ο Non-rebreathing reservoir mask approaches 0.90.

 Monitoring: May include portable chest radiographs,

periodic ABGs, regular assessments of level of sedation,

airway pressures, and functioning of ventilator alarms.

Airway Considerations

 Indications for endotracheal intubation and mechanical

ventilation include:

ο Airway obstruction due to trauma, edema, excess

secretions.

ο Apnea.
11.6

Emergency War Surgery

ο Excessive work of breathing (eg, flail chest), as indicated

by accessory muscle use, fatigue, diaphoresis, or tachypnea

when respiratory failure is imminent.

ο Decreased level of consciousness: GSC < 8.

ο Hypoxia: SaO2 < 90%, PaO2 < 60 mmHg on FIO2 > 50%.

ο Hypercarbia: PaCO2 > 60 mm Hg acutely (lower threshold

with tachypnea).

ο Shock.

ο Caution: Patients not meeting the above criteria may still

require airway protection and mechanical ventilation

preceding prolonged transport.

 Field Ventilator.

ο Impact Uni-Vent Eagle 754.

♦ Basic settings.

◊ Turn the ventilator on and set the mode using the

Mode Selector Switch (lower right). Most patients

can be well ventilated using SIMV (synchronized

intermittent mandatory ventilation).

◊ Set FIO2 using the Air/Oxygen Mixer Control, above

the Mode Selector Switch. Generally, ICU patients

should be started at an FIO2 of 1.0, and weaned as

appropriate to a level of 0.40.

◊ Set minute ventilation using Tidal Volume and

Ventilation Rate controls. The tidal volume is set at

6–10 mL/kg. Initial rate is set at 10–14 breaths/

minute and titrated to normalize PaCO2.

◊ Set positive end-expiratory pressure (PEEP) using the

PEEP Control located on the upper left of the control

panel. Initial PEEP is usually set at 5 cm H2O. Higher

values can be set in severe respiratory failure such

as adult respiratory distress syndrome (ARDS),

although generally not higher than 15 cm H2O.

Summary of typical initial settings for mechanical

ventilator: FIO2 1.0, SIMV mode, rate 12, tidal volume 800

mL, PEEP 5 cm H2O.
11.7

Critical Care

ARDS

 ARDS can start within days of injury, and should be suspected

in any casualty with:

ο Acute hypoxemia (PaO2/FIO2 ratio < 200).

ο Progressive fall in pulmonary compliance (stiff lungs,

increasing airway pressures).

ο Bilateral alveolar infiltrates on chest radiograph, with no

clinical evidence of volume overload.

Mechanical Ventilation Priorities in ARDS

 Maintain patient analgesia and sedation to prevent agitation

and ventilator/patient asynchrony.

 Keep SaO2 > 90% by increasing FIO2 and/or PEEP (maximum

15–18 cm H2O).

 Avoid prolonged FIO2 > 0.60 due to O2 toxicity.

 Avoid respiratory acidosis. Keep PaCO2 35–45 mm Hg, and

arterial blood pH > 7.25.

 Keep peak inspiratory pressure (PIP) < 40 cm H2O to prevent

iatrogenic pneumothorax and destruction of normal lung tissue.

ο Decrease tidal volume to 5–7 mL/kg.

ο Increase ventilator rate.

ο If other measures are unsuccessful, allow permissive

hypercapnia by accepting a respiratory acidosis (PaCO2

55–70 mm Hg). Use bicarb to maintain pH > 7.2.

Respiratory acidosis is less dangerous than ventilator-induced

lung injury caused by high PIP and high tidal volumes.

Cardiovascular System

 The patient who exhibits cardiovascular deterioration after

a period of apparent stability should be evaluated to rule out

the following:

ο Hypoxia or loss of airway.

ο Tension pneumothorax.

ο Recurrent bleeding from sites of injury or surgery.

ο Cardiac tamponade or direct myocardial injury.
11.8

Emergency War Surgery

ο Tachyarrhythmia.

ο Fluid loss due to “third-spacing,” burns, fever, diarrhea,

or vomiting.

ο Undiagnosed injury: intestinal injury, pancreatitis, or

infection.

ο Vasodilatation due to spinal shock, epidural anesthesia/

analgesia, and sepsis.

ο Side effect from medication.

ο GI bleeding.

ο Pulmonary embolus.

ο Abdominal compartment syndrome.

ο Excessive airway pressures from mechanical ventilation

can directly decrease cardiac ventricular function and

decrease venous preload.

 Management.

ο Support cardiovascular system by monitoring end-organ

perfusion (urine output, capillary refill) and using four

parameters of hemodynamic performance:

♦ Preload (Best index: pulmonary capillary wedge

pressure – PCWP).

♦ Afterload (systemic vascular resistance [SVR] = [MAP

– CVP]/ CO • 80).

♦ Heart rate.

♦ Cardiac contractility (best index: stroke volume; SV =

CO/h).

♦ “Make do” with the best information available—use

CVP when PA catheter unavailable.

♦ For hypovolemia and cardiovascular instability due to

sepsis:

◊ Assure adequate preload by volume repletion before

adjusting other variables (eg, adding inotropes for

low cardiac output).

◊ In other states of cardiovascular instability, the

variable manipulated is the one indicative of the

major problem.

Sinus tachycardia may be a sign of an underlying problem

(eg, hypoxia, hypovolemia, infection, or pain). Seek and

treat the primary problem, not the tachycardia.
11.9

Critical Care

 Myocardial ischemia/infarction (MI) is an uncommon

battlefield problem.

ο Suspicion is aroused when the patient exhibits angina-like

chest pain or unexplained cardiac instability (arrhythmias

or hypotension).

ο The diagnosis of an acute myocardial event is made by

the presence of ST segment elevation or depression on 12-

leak ECG and/or an abnormal elevation of serum markers

of myocardial injury (myoglobin [MB] fraction of creatine

phosphokinase, Troponin I).

 Emergency treatment for MI.

ο Supplemental O2.

ο Morphine for pain, rest.

ο Aspirin 325 mg tablet chewed and swallowed (then one

tablet PO qd).

ο NTG SL (0.4 mg tablet every 5 minutes until pain relieved,

maximum 3 doses) or IV infusion depending on severity

of condition.

ο Beta-blocker such as metoprolol (5–15 mg IV slowly q6h

or 50–100 mg PO q12h) or atenolol (50–100 mg PO) on

diagnosis and daily.

ο As resources and patient condition permit for MI with

diagnostic ECG: Optimal therapy would also include,

within 6 hours of symptoms, IV heparin and a thrombolytic

such as tissue plasminogen activator.

Renal System and Electrolytes

 Monitor urine output, blood urea nitrogen (BUN), serum

creatinine, and serum electrolytes.

 Acute renal failure (ARF) is manifested by oliguria (< 0.5 cc/

kg/h) and a rise in BUN and creatinine. The most frequent

causes for ARF are:

ο Hypovolemia.

ο Acute tubular necrosis (ATN) due to:

♦ Hypovolemia.

♦ Sepsis, IV contrast agents, aminoglycoside antibiotics,

or NSAIDs.

ο Crush, massive, soft-tissue injury or compartment syndrome,

with resultant rhabdomyolysis and myoglobinuria.
11.10

Emergency War Surgery

♦ In ARF due to rhabdomyolysis, consider administering

large volumes of IV fluid (300–800 mL/h), combined

with 50 mEq NaHCO3

/L, to alkalinize the urine with

the goal of achieving a urine output of 2.0 cc/kg/h.

♦ Bilateral renal or ureteral trauma.

Two hours of oliguria (< 20cc/h) in an ICU patient (almost

always due to inadequate resuscitation) warrants aggressive,

immediate action.

 Algorithm for hemodynamically stable ICU patient with

profound oliguria or anuria:

ο Irrigate or replace Foley catheter to ensure function.

ο After ensuring no signs of intravascular volume overload

(diffuse pulmonary crackles, S3 heart sound), administer

bolus of 1–2 L IV saline over 30 minutes.

ο Review medication list and medical history to elicit potential

factors causing ARF; stop any agents that could contribute.

ο Send any urine to lab with serum sample to calculate

fractional excretion of sodium (FENA) = (UNA • PCR)/(PNA

• UCR); FENA < 1.0 indicates prerenal cause (eg,

hypovolemia); FENA > 2.0 points to renal insult (ATN;

myoglobinuria) or postrenal cause (obstruction).

ο Consider sonogram of kidneys to rule out bilateral renal

obstruction.

ο Consider pulmonary artery catheter to optimize preload

(PCWP).

ο Once PCWP > 16–18 mm Hg, and urine output minimal/

nonexistent, administer furosemide in escalating doses IV

bolus: 40, 80, 160, 240 mg max ( > 100mg = ototoxic).

Combine last dose with single dose 1.0 g chlorothiazide

IV, or administer 10 mg metolazone PO given 30 minutes

before last dose. Also consider furosemide drip or

metolazone drip.

 If ineffective or if other complications of ARF occur, arrange

for dialysis as a temporizing renal support until spontaneous

renal recovery occurs. This means the physician must

optimize the casualty for transport out of theater, with special

attention to volume status, potassium, and acid base status.
11.11

Critical Care

ο Indications for dialysis in the casualty with ARF:

♦ Anuria beyond 8–12 hours.

♦ Hypervolemia.

♦ Hyperkalemia.

♦ Acidosis.

♦ Complications of uremia: mental status changes,

pericardial rub.

♦ Toxic levels of drugs/medications (eg, digoxin).

 Hyperkalemia.

ο Verify again hyperkalemia (serum K > 6 mEq/L) and

serum pH.

ο Give IV calcium chloride, 10 mL of 10% solution over 5

minutes.

ο Give IV NaHCO3, 50 mEq over 5 minutes.

ο Give IV Dextrose (50g D50) 50 grams + 10 units regular

insulin IV over 10 minutes.

ο Recheck K+.

ο Give beta-agonist albuterol 10–20 mg over 15 minutes by

inhalation.

ο Consider enteral K-binding with enema of sodium

polystyrene sulfonate, 25–50 g, in sorbitol.

 Hypokalemia: Treatment: 10–20 mEq KCL IV/hour in

monitored setting; difficult to treat hypokalemia unless

concomitant hypomagnesemia is first corrected.

 Hypernatremia: Usually indicative of free water deficit. Water

deficit (L) = 0.6 • weight (kg) • [(measured serum Na)/

(normal serum Na of 140) – 1]. Half of this deficit should be

replaced over first 12–24 hours, and the remainder over the

next 1–2 days.

 Hyponatremia: Indicative of excess of free water or

vasopressin (SIADH). Levels of serum sodium < 125 mEq/L

are associated with mental status changes or seizures.

Treatment should involve free water restriction or use of IV

normal saline, with goal of correction of sodium level no more

than 15 mEq/L over 24 hours, to prevent complication of

central pontine myelinolysis.

 Hypophosphatemia: Phosphate is important as an energy

source, and should be repleted to level of 2.5 mg/dL with IV

KPO4 or NaPO4, 30 mMol over 1 hour.
11.12

Emergency War Surgery

 Hyperphosphatemia (usually associated with ARF):

Phosphate levels over 6.0 mg/dL should be treated by enteral

binding agents, such as calcium acetate or sucralfate.

 Hypomagnesemia: Administer 2 g magnesium sulfate IV in

solution over 60 minutes to goal of serum level of 2.0 mEq/dL.

 Metabolic acidosis: Primarily lactic (most commonly due

to hypovolemia) and ketoacidosis. Neither should be treated

with sodium bicarbonate (it is contraindicated in lactic

acidosis). Sodium bicarbonate has very limited role in ICU

disorders: hyperkalemia, alkalinization of urine in

myoglobinuria, bicarbonate-responsive renal tubular acidosis

(RTA), and for massive gastrointestinal losses of bicarbonate

(profound diarrhea, enterocutaneous fistula).

 Metabolic alkalosis: NG suction of stomach acid causes a

hypochloremic alkalosis, responsive to replacement of NG

losses with crystalloid. Excessive loop diuretic use can also

cause metabolic (contraction) alkalosis. If further diuresis is

needed, use a carbonic anhydrase inhibitor (acetazolamide

250 mg IV every 6 h) for 1–2 days.

Hematologic System

 Most common coagulation disorder: dilutional coagulopathy.

ο Others include heparin-induced thrombocytopenia,

disseminated intravascular coagulation, coagulopathy due

to hypothermia or diffuse hepatic damage, and

thrombocytopenia.

ο Most require replacement transfusion of appropriate blood

products.

 To prevent trauma-related deep venous thrombosis (DVT)

and pulmonary embolism, prophylactic measures

(subcutaneous heparin or sequential compression devices)

are required.

Gastrointestinal System and Nutrition

 Prolonged shock can lead to GI dysfunction.

ο Stress gastritis: Increased risk of severe head injuries or

burns, mechanical ventilation, systemic anticoagulation

therapy, or sepsis. Prevention: sucralfate, histamine-2

receptor antagonist (eg, ranitidine) or a proton pump

inhibitor (eg, omeprazole).
11.13

Critical Care

ο Acalculous cholecystitis: Suspect with right upper quadrant

abdominal pain, abnormalities in liver function tests, or

fever/leukocytosis of unclear cause. Ultrasound shows

gallbladder inflammation with wall thickening or

pericholecystic fluid. Treatment: broad-spectrum antibiotics

and ultrasound-guided percutaneous drainage or operation.

ο Hepatic failure portends a dire prognosis. Initial signs

include hyperbilirubinemia, elevation of the prothrombin

time, hypoalbuminemia, profound hypoglycemia,

obtundation. Massive amounts of fresh frozen plasma are

required to prevent exsanguination from coagulopathy.

 Nutrition can prove problematic in the battlefield ICU patient.

ο Systemic inflammation induced by severe injury often

results in catabolism and protein wasting, making early

nutritional support imperative.

ο Nutrition should commence within 24–48 hours of injury.

ο Enteral feedings are superior to parenteral nutrition (TPN),

offering a lower infection rate and shorter ICU stays.

ο The following goals serve to guide nutritional

management:

♦ Caloric requirement: 25–30 kcal/kg/d.

♦ Protein requirement: 1.0–1.5 g/kg/d.

♦ 30%–40% of total caloric intake per day should be as fat.

ο Nutrition should include a balanced electrolyte solution

containing supplemental potassium, calcium, magnesium,

phosphate, multivitamins and trace elements (zinc, copper,

manganese, and chromium).

ο The two most common problems associated with enteral

nutrition are diarrhea and aspiration.

♦ Aspiration can be associated with severe pneumonitis,

but can be prevented by:

◊ Keeping the head of the bed up.

◊ Feeding into the jejunum or duodenum rather than

the stomach.

◊ Checking gastric residuals every 4 hours (feedings

should be stopped if residual greater than 200 mL).

♦ Diarrhea can be alleviated by:

◊ Decreasing the osmolarity of the enteral solution.

◊ Adding fiber.

◊ Agents such as loperamide in small doses.
11.14

Emergency War Surgery

Immune System and Infections

 Differential diagnosis of ICU infections.

ο Pneumonia (nosocomial or aspiration).

ο Central venous catheter infection – if considered, remove

catheter.

ο UTI.

ο Wound or soft-tissue infection.

ο Intra-abdominal abscess (especially following

laparotomy).

ο Systemic fungal infection.

ο Sinusitis.

ο Acalculous cholecystitis.

ο Pancreatitis.

 Prophylactic antibiotics.

ο A short course of prophylactic antibiotics (24–48 h) is

warranted after penetrating injury on the battlefield.

ο After this, antibiotics should be withheld unless a

documented infection is confirmed, or a severe deterioration

in clinical status suggestive of sepsis is encountered.

ο Sepsis warrants a short course of broad spectrum IV

antibiotics, but they must be stopped in 72 hours if no

microbiologic pathogens are confirmed by culture.

ο Fever and leukocytosis, by themselves, are not sufficient

justification for antibiotics.

Endocrine System

 Hyperglycemia.

ο Control, to prevent ketoacidosis, hyperosmolar coma, and

intravascular volume loss due to osmotic diuresis.

ο The two most common causes are uncontrolled or

unrecognized infections and the use of TPN.

ο The best technique for control of hyperglycemia is a constant

IV infusion of insulin, usually 1.0–10 units per hour.

♦ Due to frequent problems with patient perfusion,

subcutaneous injections are less reliable in the ICU patient.

♦ Patients with profound hyperglycemia (serum glucose >

800 mg/dL) and volume depletion, due to osmotic

diuresis, should receive fluid resuscitation with crystalloid
11.15

Critical Care

before receiving insulin, to prevent further shifts in

intravascular volume as the glucose shifts intracellularly.

♦ Limit correction rate to 100 mg/dL per hour (700 mg/dL

takes 7 h to correct) and assess for resultant hypokalemia.

 Corticosteroids are rarely indicated after major trauma.

ο There is no proven benefit to steroid treatment for closed

head injury or sepsis.

ο Steroids are indicated for proven adrenocortical deficiency

(a rare occurrence among battlefield casualties) and spinal

cord injury with neurologic deficit.

Musculoskeletal System

 Monitor for the development of compartment syndrome,

vascular ischemia, and rhabdomyolysis.

 Distal extremities should be assessed regularly for

neurovascular status: presence of pulses, sensation, motor

function, warmth, and skin color.

Preparation for Evacuation

 Optimally, the combat casualty will be medically stabilized

before transport out of theater.

ο Native or mechanical airway is maintained.

ο Sufficient blood pressure, to allow organ perfusion, that

has been stable for at least 8 hours.

ο Both primary and secondary phases of shock resuscitation

have been completed.

ο All sources of bleeding have been identified and controlled.

ο Life-saving or definitive surgery not required for the next

24 hours.

 Transfer out of a battlefield ICU requires a USAF Critical Care

Air Transport Team (CCATT) with physician-to-physician

and nurse-to-nurse communication to summarize condition

of the patient, operations performed, treatment being given,

and support required during flight (in particular, need for

oxygen, mechanical ventilation, suction, blood products, and

monitoring).

 Copies of medical records, radiographs, 3 days of IV fluid,

and all medications should accompany the patient.
11.16

Emergency War Surgery