Emergency War Surgery (2004)

Emergency War Surgery

Table 9-1. Induction Agents and Sedatives.

Agent

Routine Dose*

Characteristics

Concerns

Ketamine

1.0-2.0 mg/kg IV

Dissociative anesthetic

Varying degrees

and amnestic.

of purposeful

Sympathomimetic

skeletal move-

effects (useful in

ment despite

hypovolemia).

intense

Potent bronchodilator.

analgesia

and amnesia.

4.0-8.0 mg/kg

Onset within 30-60 sec.

Increased

Emergence delirium

salivation,

avoided with con-

consider an

comitant benzodia-

antisialagogue.

zepine use.

Barbiturates

3-5 mg/kg

Onset within 30-60

May cause

(eg, thiopental)

seconds.

profound

hypotension in

hypovolemic

shock patients.

Propofol

1.5-2.5 mg/kg

Mixed in lipid, strict

Contraindicated

sterility must be

in acute

ensured.

hypovolemic

Rapid onset and rapidly

shock patients.

metabolized.

Onset within 30-60

seconds.

Etomidate

0.2-0.4 mg/kg

Onset within 30-60

May cause

seconds.

clonus.

Duration 3-10 min.

Minimal cardiac effects.

Minimal effects on

peripheral and

pulmonary circulation.

Maintains cerebral

perfusion.

* All induction agents can be used for induction of severely injured patients

if reduced dosages are used (eg, ¹/2 of the lower recommended dose).

However, the recommended choice for hypovolemic patients would be

Ketamine > etomidate >> thiopental > propofol.

9.4

Anesthesia

Rapid Sequence Intubation (RSI) 7 steps*

1. Preoxygenate with 100% oxygen by mask.

2. Consider fentanyl—titrate to maintain adequate blood

pressure and effect (2.0-2.5 µg/kg).

3. Cricoid pressure—Sellick maneuver until endotracheal

tube (ETT) placement is confirmed and balloon is

inflated.

4. Induction agent: etomidate 0.1-0.4 mg/kg IV push.

5. Muscle relaxant: succinylcholine 1.0-1.5 mg/kg IV push.

6. Laryngoscopy and orotracheal intubation.

7. Verify tube placement.

*For children, see page 33.6.

Endotracheal intubation.

Orotracheal.

♦ Direct laryngoscopy 60-90 seconds after administration

of induction agents and neuromuscular blockade.

♦ First attempt is the best chance for success, but have a

backup plan:

◊ Optimize positioning of patient and anesthesia

provider.

◊ Have adjuncts readily available (stylet, smaller

diameter tubes, alternative laryngoscope blades,

suction, laryngeal mask airway, lighted stylet).

Nasotracheal should generally not be performed.

Other considerations.

♦ Maintain cricoid pressure until balloon inflated and tube

position is confirmed.

♦ Hypertension can be managed with short-acting

medications such as beta blockers (labetalol, esmolol)

or sodium nitroprusside.

♦ May treat induction-related (transient) hypotension

initially with small dose of ephedrine (5-10mg) or

Neosynephrine (50 µg), but if hypotension persists after

induction agents are metabolized, use fluids to treat the

persistent hypovolemia. The anesthesiologist must

convey this situation to the surgeon, as the need to

control bleeding becomes urgent.

9.5

Emergency War Surgery

♦ A sensitive airway can be topically anesthetized with

lidocaine 1.5 mg/kg 1-2 minutes before laryngoscopy.

Verify ETT placement.

ο Auscultate the lungs.

ο Measure the end-tidal CO₂.

ο Ensure that the SaO

remains high.

ο Palpate cuff of ETT in sternal notch.

ο Place the chemical CO₂ sensors in the airway circuit.

Verification of tube placement is VITAL. Any difficulty

with oxygenation/ventilation following RSI should

prompt evaluation for immediate reintubation.

The Difficult Airway (see Chapter 5, Airway and Breathing)

Initially provide airway management with jaw-thrust, facemask

oxygenation, and assess the situation. Failed RSI may be due to

inadequate time for induction agents to work; inadequate time

for muscle relaxation to occur; anatomically difficult airway; or

obstruction due to secretions, blood, trauma, or foreign material.

Resume oxygenation; consider placing a temporary oral airway.

Reposition patient and anesthesia provider.

Call for help.

Consider alternatives to RSI.

ο Awake intubation.

ο Laryngeal mask airway.

ο Regional anesthesia or local anesthesia.

ο Surgical airway.

Maintenance of General Anesthesia

General Anesthesia Is Maintained After Intubation With

Oxygen. Titrate to maintain SaO

> 92%.

Ventilation.

ο Tidal volume (TV) 10-15 cc/kg.

ο Respiratory rate (RR) 6-10/min.

ο PEEP (positive end-expiratory pressure) if desired at 5 cm

H₂O, titrate as necessary.

Minimal alveolar concentration (MAC).

ο 0.3-0.5 MAC: awareness abolished although 50% of

patients respond to verbal commands.

9.6

Anesthesia

ο 1 MAC: 50% of patients do not move to surgical stimulus.

ο 1.2 MAC: 95% of patients do not move to surgical stimulus.

ο Common inhalation agent MACs:

♦ Halothane: 0.75%.

♦ Sevoflurane: 1.8%.

♦ Isoflurane: 1.17%.

♦ Enflurane: 1.63%.

♦ Nitrous Oxide (N₂O) = 104%.

♦ Additive effects (eg, 60% N₂O mixed with 0.8%

sevoflurane yields 1 MAC).

Total intravenous anesthesia (TIVA).

ο Mix midazolam 5 mg, vecuronium 10 mg, ketamine 200

mg in 50 cc normal saline (NS) and infuse at 0.5 cc/kg/h

(stop 10-15 minutes before end of surgery).

ο Mix 50-100 µg of ketamine with 500 mg of propofol (50 cc

of 10% propofol) and administer at 50-100 µg/kg/min (21-

42 mL/h for a 70 kg patient).

Balanced anesthesia (titration of drugs and gases) combine:

ο 0.4 MAC.

ο Versed 1-2 mg/h.

ο Ketamine 2-4 mg/kg/h.

Conclusion of General Anesthesia

If the patient is to remain intubated, anesthetics may be term-

inated but sedatives and muscle relaxants are maintained.

If the patient is to be extubated, ventilation is decreased to

allow the patient to spontaneously breathe.

ο Anesthetic agents are stopped 5 minutes before conclusion

of surgery.

ο Glycopyrrolate (Robinul) (0.01-0.02 mg/kg IV over 3-5

minutes) to decrease parasympathetic stimulation and

secretions. This can be administered at the same time or

before neostigmine.

ο Muscle relaxation reversal with neostigmine (0.04-0.08

mg/kg IV over 3-5 minutes, can be mixed in same syringe

as glycopyrrolate).

Extubation criteria include reversal of muscle relaxation,

spontaneous ventilation, response to commands, eye

9.7

Emergency War Surgery

opening, and head lifting for 5 seconds. When in doubt, keep

the patient intubated.

Amnestic therapy with midazolam and analgesic therapy

with a narcotic is appropriate in small amounts so as not to

eliminate the spontaneous respiratory drive.

Regional Anesthesia

Regional anesthesia (RA) is a “field friendly” anesthetic requiring

minimal logistical support while providing quality anesthesia

and analgesia on the battlefield. Advantages of RA on the

modern battlefield are listed below.

Excellent operating conditions.

Profound perioperative analgesia.

Stable hemodynamics.

Limb specific anesthesia.

Reduced need for other anesthetics.

Improved postoperative alertness.

Minimal side effects.

Rapid recovery from anesthesia.

Simple, easily transported equipment needed.

Recent conflicts have revealed that the majority of casualties will

have superficial wounds or wounds of the extremities. RA is well

suited for the management of these injuries either as an adjunct to

general anesthesia or as the primary anesthetic. The use of basic

RA blocks is encouraged when time and resources are available.

Superficial cervical plexus block.

Axillary brachial plexus block.

IV regional anesthesia.

Wrist block.

Digital nerve block.

Intercostobrachial nerve block.

Saphenous nerve block.

Ankle block.

Spinal anesthesia.

Lumbar epidural anesthesia.

Combined spinal-epidural anesthesia.

Femoral nerve block.

9.8

Anesthesia

Prior training in basic block techniques is implied, and use of a

nerve stimulator, when appropriate, is encouraged to enhance

block success. More advanced blocks and continuous peripheral

nerve blocks are typically not available until the patient arrives

at a combat support hospital (CSH) or higher level health care

facility where personnel trained in these techniques are

available. A long-acting local anesthetic such as 0.5% ropivacaine

is used for most single-injection peripheral nerve blocks.

Peripheral nerve blocks can often be used to treat pain (without

the respiratory depression of narcotics) while patients are

waiting for surgery.

Neuraxial anesthesia.

ο Subarachnoid block (SAB).

ο Epidural block.

When the patient’s physical condition allows the use of spinal

or epidural anesthesia those techniques are encouraged. The

sympathectomy that results is often poorly tolerated in a trauma

patient and this must be factored into any decision to use those

techniques. Peripheral nerve blocks do not have this limitation.

Local anesthesia.

When local anesthesia would suffice, such as in certain wound

debridements and wound closures, it should be the technique

of choice.

Field Anesthesia Equipment

There are two anesthesia apparatuses currently fielded in the

forward surgical environment: (1) the draw-over vaporizer and

(2) a conventional portable ventilator machine. A schematic of

the draw-over system is shown in Figure 9-1.

Draw-over vaporizer.

ο Currently fielded model: Ohmeda Portable Anesthesia

Complete (PAC).

ο Demand type system (unlike the plenum systems in

hospital-based ORs).

♦ When the patient does not initiate a breath or the self-

inflating bag is not squeezed, there is no flow of gas.

No demand equals no flow.

ο Temperature-compensated flow-over in-line vaporizer.

9.9

Emergency War Surgery

150

Fig. 9-1. Draw-over apparatus in combination with the ventilator.

ο Optimal oxygen conservation requires a larger reservoir

(oxygen economizer tube [OET]) than is described in the

operator’s manual — a 3.5 ft OET optimizes FIO

ο May be used with spontaneous or controlled ventilations.

ο Bolted-on performance chart outlines dial positions for

some commonly used anesthetics (eg, halothane, isoflu-

rane, enflurane, and ether). Ether is highly flammable;

use extreme care.

Ohmeda UPAC Draw-Over Apparatus in Combination With

the Impact Uni-Vent Eagle 754 Portable Ventilator:

Currently, there is no mechanical ventilator specifically

designed for use with the UPAC draw-over apparatus, but

use with various portable ventilators has been studied in both

the draw-over and push-over configuration.

ο Adding the ventilator frees the anesthesia provider’s hands

while providing more uniform ventilation and more

consistent concentrations of the inhalational anesthetic

agent.

9.10

Anesthesia

ο The draw-over configuration places the ventilator distal

to the vaporizer, entraining ambient air and vapor across

the vaporizer in the same manner as the spontaneously

breathing patient. Do not attach a compressed source of

air to the Impact Uni-Vent Eagle 754 in this configuration

because the Uni-Vent Eagle 754 will preferentially deliver

the compressed gases and will not entrain air/anesthetic

gases from the UPAC draw-over.

ο The push-over configuration places the ventilator proximal

to the vaporizer, effectively pushing entrained ambient air

across the vaporizer and then to the patient.

The Impact Uni-Vent Eagle 754 portable ventilator (Figure 9-1)

is not part of the UPAC apparatus but is standard equipment

for the US military. It has been used in combination with the

Ohmeda UPAC Draw-Over Apparatus.

The air-entrainment (side intake) port is used to create the

draw-over/ventilator combination.

♦ The side intake port of the ventilator contains a

nonreturn valve preventing back pressure on the

vaporizer which could result in erratic and inconsistent

anesthetic agent concentrations.

The patient air-outlet port on the ventilator also contains

a nonreturn valve, preventing back flow into the ventilator

from the patient side.

Scavenging of waste gases can be accomplished by

attaching corrugated anesthesia tubing to either the outlet

port of the Ambu-E valve (induction circuit) or the

exhalation port of the ventilator tubing (ventilator circuit)

venting to the outside atmosphere.

The following items are added to the circuit to improve this

UPAC/Impact Uni-Vent Eagle 754 ventilator combination:

♦ Small and large circuit adapters to aid in attachment of

various pieces.

♦ PALL Heat and Moisture Exchange Filter to conserve

heat and limit patient contact with the circuit.

♦ Accordion circuit extender to move the weight of the

circuit away from the patient connection.

♦ O₂ extension tubing to attach supplemental O₂.

9.11

Emergency War Surgery

ο Two separate circuits should be constructed for use with

the UPACTM/Uni-Vent Eagle 754 combination: one for

induction and spontaneous ventilation and the second for

controlled ventilation using the portable ventilator.

♦ This process can be complicated because switching

circuit components requires several disconnections and

reconnections, creating the potential for error. (Practice.)

Conventional plenum anesthesia machine.

ο Currently fielded models: Drager Narkomed and Magellan

2000.

ο Compact version of standard OR machines, with com-

parable capabilities.

9.12

Chapter 10

Infections

Introduction

All wounds incurred on the battlefield are grossly

contaminated with bacteria. Most will become infected

unless appropriate treatment is initiated quickly.

The battlefield environment is conducive to wound infection

due to

Absence of “sterile” wounding agents on the battlefield. All

foreign bodies (wounding projectile fragments, clothing, dirt)

are contaminated with bacteria.

High-energy projectile wounding (devitalized tissue,

hematoma, tissue ischemia).

Delay in casualty evacuation.

Diagnosis of a Wound Infection

The four “-ors:” dolor, rubor, calor, and tumor—pain and

tenderness, redness, warmth, and swelling.

Drainage or discharge, ranging from frank pus to the foul

“dishwater” discharge of clostridial infection.

Crepitus, radiographic evidence of soft-tissue gas, epidermal

blistering, and/or epidermal necrosis are the hallmarks of

necrotizing soft tissue infection, such as clostridial gas

gangrene or necrotizing fasciitis.

Systemic effects such as fever, leukocytosis, unexplained

tachycardia, or hypotension.

Confirm diagnosis by Gram stain and culture, if available,

and/or tissue biopsy.

10.1

Emergency War Surgery

Common Microorganisms Causing Battlefield Infections

Gram-positive cocci: staphylococci, streptococci, and

enterococci.

Gram-negative rods: Escherichia Coli, Proteus, and Klebsiella.

ο Pseudomonas, Enterobacter, Acinetobacter, and Serratia are

common nosocomial pathogens usually expected among

casualties who have been hospitalized for an extended

period, not those fresh off the battlefield.

Salmonella, Shigella, and Vibrio should be suspected in cases

of bacterial dysentery.

Anaerobic Gram-positive and Gram-negative rods: Clostridia,

Bacteroides, and Prevotella species.

Fungal species: Candida species should be suspected in casualties

hospitalized for prolonged periods, those malnourished or

immunosuppressed, or those who have received broad

spectrum antibiotics, adrenocortical steroids, or parenteral

nutrition. Empiric therapy should be considered in appropriate

patients with presumptive evidence of fungal infection.

The greatest threat of infection to the wounded battlefield

casualty is the development of clostridial myonecrosis (gas

gangrene), commonly due to Clostridium perfringens.

Common Patterns of Infection

Skin, soft tissue, muscle, and bone: Primarily due to

staphylococcal, streptococcal, and clostridial species. These

infections include wound abscess, cellulitis, septic arthritis,

osteomyelitis, necrotizing fasciitis, and gas gangrene.

Clostridium tetani can enter through any wound—even

minor burns and corneal abrasions. Prophylaxis is required

to prevent tetanus toxemia.

Intracranial: Meningitis, encephalitis, and abscess,

commonly due to staphylococci and Gram-negative rods,

which are difficult to treat due to the impervious nature of

the meninges to common antibiotics.

10.2

Infections

Orofacial and neck: Gram-positive cocci and mouth

anaerobes, generally responsive to surgery and clindamycin.

Thoracic cavity: Empyema (usually staphylococcal) and

pneumonia (Staphylococcus, Streptococcus, Pseudomonas),

especially among those on prolonged mechanical ventilation

or those casualties prone to aspiration (polymicrobial).

Intraabdominal: Include posttraumatic or post-operative

abscess, and peritonitis due to Enterococcus, Gram-negative

rods, and anaerobic bacilli. Clostridium difficile is often

responsible for a potentially severe diarrheal colitis that

occurs following the administration of even one dose of

antibiotic.

Systemic sepsis: A syndrome caused by a bloodborne or

severe regional infection resulting in a global inflammatory

response (fever, leukocytosis, tachycardia, tachypnea, and

possibly hypotension).

ο A similar inflammatory response without infection can be

caused by a focus of retained necrotic tissue, or the mere

act of sustaining severe trauma.

ο Culprit microorganisms will not be recovered in all cases

of sepsis syndrome.

ο Although typically associated with Gram-negative

organisms, any bacterial or fungal agent can cause sepsis.

Prompt surgical debridement is the cornerstone of

prophylaxis/treatment of war wound infections.

Treatment

General Principles

Surgical and antibiotic treatment should begin early and be

repeated in the prophylaxis of war wound infection.

Optimally, surgical debridement should be achieved within

6 hours of injury.

Following initial exploration and debridement, the wound

should be sufficiently irrigated to ensure all dead material,

bacterial contamination, and foreign material has been

washed from the wound.

10.3

Emergency War Surgery

Excessive irrigation, especially under pressure, should be

avoided, because this can dilute the body’s natural immune

cellular defenses and contribute to bacteremia.

The skin is left open, and a lightly moistened sterile gauze

dressing is applied.

Antibiotics should be started ASAP after wounding, then

continued for 24 hours, depending on the size, extent of

destruction, and degree of contamination of the wound.

ο If time from wounding to initiation of antibiotics is > 6

hours, or time from wounding to surgery is > 12 hours,

give antibiotics using regimen for established infection.

The choice of empiric antibiotic is dependent on the part of

the body injured (Table 10-1).

Once a battlefield wound has become infected, treatment is

two-fold—surgical and medical.

ο Surgical strategy remains the same: Open the wound, remove

infected and necrotic tissue, and inspect for foreign material.

ο Drainage is generally employed in abscess cavities to

prevent premature closure and reformation.

ο Empiric broad-spectrum antibiotic therapy is initiated

against likely pathogens and continued for 7 to 10 days.

ο Ideally, obtain cultures and tailor therapy to cover the

actual pathogens recovered on Gram stain and culture.

Routine bacteriology is often not available in forward

medical facilities.

ο Because Bacteroides and Clostridia are difficult to culture,

tailor antibiotic therapy to cover these organisms.

ο If the debrided wound still has possibly ischemic tissue or

retained foreign material, the patient is returned to the OR

every 1 to 2 days for redebridement, until absolute

assurance of healthy, clean tissue is achieved.

Specific Infections

Tetanus.

ο Battlefield wounds are “tetanus-prone” due to high levels

of contamination with Clostridium tetani.

ο Bacteria grow anaerobically and release a CNS toxin that

results in muscle spasm, trismus, neck rigidity, and back

arching.

10.4

Table 10-1. Empiric Antibiotic Coverage for War Injuries.

Site of Injury

Empiric Antibiotic

Covered Organisms

Cranium/penetrating

Ancef/Vanc + Flagyl

Gram positives + anaerobes

injury

brain injury

Maxillofacial

Ancef + clindamycin

Gram positives + anaerobes

Neck

Ancef

Skin flora

Chest

Ancef

Skin flora

Abdomen

Liver

Fluoroquinolone/2nd generation

Gram negatives, gram positives,

cephalosporin

+ anaerobes

Gastrointestinal tract

Carbapenam/penicillin (Zosyn)

“

with gross contamination

Gastrointestinal tract

2nd generation cephalosporin

“

without gross contamination

Genitourinary

Aminoglycoside + 2nd generation

“

cephalosporin

Spleen

2nd generation cephalosporin +

“

fluoroquinolone + immunize splenectomy

patients later for encapsulated organisms

Pelvic

With gastrointestinal injury

Carbepenam or combo penicillin

Gut flora + anaerobes

No gastrointestinal injury

2nd generation cephalosporin

Skin organisms

Extremity

Soft tissue only

Ancef or 2nd generation cephalosporin

+ aminoglycoside

Bone/vascular involvement

2nd generation cephalosporin +

aminoglycoside and fluoroquinolone

Treat gross contamination of any wound with debris from uniforms and the environment with broad spectrum Gram-negative and

anaerobic coverage regardless of area of injury, eg, Ancef + penicillin + gentamicin; or Unasyn alone.

Emergency War Surgery

In addition to surgical debridement of war wounds,

additional prophylactic measures for tetanus-prone

wounds include

♦ Administration of 0.5ml IM of tetanus toxoid if prior

tetanus immunization is uncertain, less than three doses,

or more than five years since last dose.

♦ Administration of 250-500 units IM of tetanus immune

globulin in a separate syringe and at a separate site from

the toxoid if prior tetanus immunization is uncertain

or less than three doses.

Treatment for established tetanus includes

♦ IV antibiotics (penicillin G, 24 million U/d; or

doxycycline, 100 mg bid; or metronidazole, 500 mg q6h

for 7 days).

♦ Tetanus immune globulin.

♦ Wound debridement as needed.

♦ IV diazepam to ameliorate the muscle spasm.

♦ Place patient in a dark, quiet room free of extraneous

stimulation.

♦ May warrant endotracheal intubation, mechanical

ventilation, and neuromuscular blockade.

Soft-tissue infections.

ο Cellulitis is manifested by localized skin erythema, heat,

tenderness, and swelling or induration.

♦ Treatment: IV antibiotics against streptococcal and

staphylococcal species (IV nafcillin, cefazolin or, in the

penicillin-allergic patient, clindamycin or vancomycin).

ο Post-operative wound infections become evident by

wound pain, redness, swelling, warmth, and/or foul or

purulent discharge, with fever and/or leukocytosis.

♦ Treatment: Open the wound, drain the infected fluid,

and debride any necrotic tissue present.

♦ The wound is left open and allowed to close via

secondary intention.

ο Necrotizing soft tissue infections are the most dreaded

infections resulting from battlefield wounding. These

include clostridial myonecrosis (gas gangrene) and

polymicrobial infections caused by Streptococcus,

Staphylococcus, Enterococcus, Enterobacteriaceae, Bacteroides,

and Clostridia.

10.6

Infections

♦ The organisms create a rapidly advancing infection

within the subcutaneous tissues and/or muscle by

producing exotoxins that lead to bacteremia, toxemia,

and septic shock.

♦ All layers of soft tissue can be involved, including skin

(blistering and necrosis), subcutaneous tissue

(panniculitis), fascia (fasciitis), and muscle.

♦ Clinical manifestations begin locally with severe pain,

crepitus, and with clostridia, a thin, brown, foul-

smelling discharge.

♦ The skin may be tense and shiny, showing pallor or a

bronze color.

♦ Systemic signs include fever, leukocytosis, mental

obtundation, hemolytic anemia, and hypotension,

progressing rapidly to multiple organ failure and death

in untreated or under-treated cases.

♦ The diagnosis is made by history of severe unexpected

wound pain combined with palpable or radiographic

soft tissue gas (air in subcutaneous tissue and/or

muscle).

♦ Absence of soft-tissue gas does not exclude diagnosis

of necrotizing infection.

♦ Treatment is surgical, including early, comprehensive,

and repeated (every 24-48 hours) debridement of all

dead and infected tissue, combined with antibiotics.

♦ Excision of affected tissue must be as radical as

necessary (including amputation or disarticulation) to

remove all muscle that is discolored, noncontractile,

nonbleeding, or suspicious.

♦ Identification of causative organisms often problematic:

Treatment must be aimed at all possible organisms.

♦ IV antibiotic therapy.

♦ Clindamycin, 900 mg q8h; plus penicillin G, 4 million

U q4; plus gentamicin, 5-7 mg/kg qd.

◊ As a substitute for clindamycin: metronidazole, 500

mg q6h.

◊ As a substitute for penicillin: ceftriaxone, 2.0 g q12h,

or erythromycin 1.0 g q6h.

◊ As a substitute for gentamicin: ciprofloxacin, 400 mg

q12h.

10.7

Emergency War Surgery

♦ Alternative regimen: penicillin G, 4 million U q4h plus

imipenem, 500 mg q6h.

Intraabdominal infections.

♦ Prevention.

♦ Regimens (start ASAP, continue x 24 hours post-op).

◊ Single agent: cefotetan 1.0 g q12h, or ampicillin/

sulbactam, 3 g q6h, or cefoxitin, 1.0 g q8h.

◊ Triple agent: ampicillin 2 g q6h; plus anaerobic coverage

(metronidazole, 500 mg q6h; or clindamycin, 900 mg

q8h); plus gentamicin 5-7 mg/kg qd.

♦ Established intraabdominal infection (peritonitis or

abscess).

♦ Same regimen as above, except continue for 7 to 10 days.

♦ Drain all abscesses.

Pulmonary infections.

♦ Empyema (generally Streptococcal) following penetrating

thoracic trauma is typically due to contamination from

the projectile, chest tubes, or thoracotomy.

♦ Diagnosis: Loculations, air/fluid levels on radiograph,

pleural aspirate.

♦ Treatment.

◊ Chest tube initially, and thoracotomy if unsuccessful.

◊ Cefotaxime, or ceftriaxone, or cefoxitin, or imipenem.

♦ Pneumonia is most frequently due to aspiration (eg,

patients with head injury) and prolonged mechanical

ventilation.

♦ The diagnosis is made through radiograph finding of a

new pulmonary infiltrate that does not clear with chest

physiotherapy, combined with

◊ Fever or leukocytosis.

◊ Sputum analysis showing copious bacteria and

leukocytes.

♦ Empiric therapy is directed toward likely pathogens.

◊ Aspiration: Streptococcal pneumonia, coliforms, and

oral anaerobes are likely. IV antibiotics such as

ampicillin/sulbactam, clindamycin, or cefoxitin have

proven effective.

◊ Ventilator-associated pneumonia: staphylococcus,

Pseudomonas, and other nosocomial Enterobacteriaceae.

Broad coverage is best with such agents as imipenem,

10.8

Infections

ciprofloxacin, vancomycin, and/or ceftazidime, plus

an aminoglycoside.

Systemic Sepsis

Sepsis can be defined as infection combined with a prolonged

systemic inflammatory response that includes two or more of

the following conditions.

Tachycardia.

Fever or hypothermia.

Tachypnea or hyperventilation.

Leukocytosis or acute leukopenia.

Progression to septic shock is manifest by systemic

hypoperfusion: profound hypotension, mental obtundation, or

lactic acidosis. Treatment is a three-pronged approach:

Identify and eradicate the source.

Broad-spectrum intravenous antibiotics for the most likely

pathogens.

ICU support for failing organ systems, such as cardiovascular

collapse, acute renal failure, and respiratory failure.

It is often difficult to identify the source of sepsis, but it is the

most important factor in determining the outcome. Potential

sources of occult infection include

An undrained collection of pus such as a wound infection,

intraabdominal abscess, sinusitis, or perianal abscess.

Ventilator-associated pneumonia.

Urinary tract infection.

Disseminated fungal infection.

Central intravenous catheter infection.

Acalculous cholecystitis.

Intensive care support for sepsis involves vigorous resuscitation

to restore perfusion to prevent multiple organ dysfunction.

This requires optimization of hemodynamic parameters

(pulmonary artery occlusion pressure, cardiac output, and

oxygen delivery) to reverse anaerobic metabolism and lactic

acidosis. Endpoints of resuscitation, such as urine output,

base deficit, and blood lactate levels guide successful

treatment. Until the source for sepsis is identified and actual

pathogens isolated, empiric therapy with broad-spectrum

intravenous antibiotics is warranted. Suitable regimens might

include

10.9

Emergency War Surgery

Imipenem, 500 mg q6h.

Piperacillin and tazobactam (Zosyn), 3.375 g q6h; or

ceftazidime, 2.0 g q8h; or cefepime, 2.0 g q12h; PLUS

gentamicin, 5-7 mg/kg qd (based on once-daily dosing

strategy and no renal impairment); or ciprofloxacin, 400 mg

q12h.

Addition of vancomycin, 1.0 g q12h if methicillin-resistant

Staphylococcus aureus is a likely pathogen.

Addition of linezolid, 600 mg q12h if vancomycin-resistant

enterococcus (VRE) is a likely pathogen.

Conclusion

Battlefield casualties are at high risk for infection. In particular,

war wounds are predisposed to infection due to environmental

conditions on the battlefield, devitalized tissue, and foreign

bodies in the wound. The key to avoiding wound infection is

prompt and adequate wound exploration, removal of all foreign

material, and excision of all dead tissue. All battlefield wounds

and incisions should have the skin left open. Antibiotics play

an adjunctive role in the prophylaxis of wound and other

infections in the battlefield MTF. Knowledge of likely pathogens

for particular infections and sites, as well as optimal antibiotics

to eradicate those pathogens (Table 10-2), will aid the battlefield

clinician in averting and treating infections.

10.10

Table 10-2. Spectrum and Dosage of Selected Antibiotic Agents.

Agent

Antibacterial Spectrum

Dosage

Penicillin G

Streptococcus pyogenes, penicillin-sensitive Streptococcus pneumonia,

4 mil U IV q4h

clostridial sp

Ampicillin

Enterococcal sp, streptococcal sp, Proteus, some E coli, Klebsiella

2 g IV q6h

Ampicillin/

Enterococcal sp, streptococcal sp, Staphylococcus,* E coli,

3 g IV q6h

sulbactam

Proteus, Klebsiella, Clostridial sp, Bacteroides/Prevotella sp

Nafcillin

Staphylococcal sp,* streptococcal sp

1 g IV q4h

Piperacillin/

Enterococcal sp, streptococcal sp, Staphylococcus,* E coli, Pseudomonas

3.375 g IV q6h

tazobactam

and other enterobacteriaceae, clostridial sp, Bacteroides/Prevotella sp

Imipenem

Enterococcal sp, streptococcal sp, Staphylococcus,* E coli, Pseudomonas

500 mg IV q6h

and other enterobacteriaceae, clostridial sp, Bacteroides/Prevotella sp

Cefazolin

Staphylococcal sp,* streptococcal sp, E coli, Klebsiella, Proteus

1.0 g IV q8h

Cefoxitin

Staphylococcal sp,* streptococcal sp, E coli and similar enterobacteriaceae,

1.0 g IV q6h

clostridial sp, Bacteroides/Prevotella sp

Ceftazidime

Streptococcal sp, E coli, Pseudomonas and other enterobacteriaceae

2.0 g q8h

Ceftriaxone

Streptococcal sp, staphylococcal sp,* Neisseria sp, E coli and most

2.0 g q12h

enterobacteriaceae (NOT Pseudomonas), clostridial sp

Ciprofloxacin

E coli, Pseudomonas and other enterobacteriaceae

400 mg q12h

Gentamycin

E coli, Pseudomonas and other enterobacteriaceae

5-7 mg/kg qd (based on once-

daily dosing strategy and no

renal impairment)

Vancomycin

Streptococcal, enterococcal, and staphylococcal species (including MRSA;

1.0 g q12h

not VRE)

Erythromycin

Streptococcal sp, clostridial sp

0.5-1.0 g q6h

Clindamycin

Streptococcus sp, Staphylococcus sp,* clostridial sp, Bacteroides, and Prevotella sp

900 mg q8h

Metronidazole

Clostridial sp, Bacteroides and Prevotella sp

500 mg q6h

*Not methicillin resistant Staphylococcus aureaus (MRSA)

Dosage and dosage intervals are average recommendations. Individual dosing may vary.

Chapter 11

Critical Care

Introduction

Each battlefield ICU should have a dedicated intensive care

physician, due to the severity and lethality of blast and high-

velocity 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.

11.1

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.

11.2

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.

11.3

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.

11.4

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 head-

injured 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.

11.5

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.

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.

11.6

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.

11.7

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.

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.

11.8

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.

11.9

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:

Irrigate or replace Foley catheter to ensure function.

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.

Review medication list and medical history to elicit potential

factors causing ARF; stop any agents that could contribute.

Send any urine to lab with serum sample to calculate

fractional excretion of sodium (FENA) = (U_NA • P_CR)/(P_NA

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

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

myoglobinuria) or postrenal cause (obstruction).

Consider sonogram of kidneys to rule out bilateral renal

obstruction.

Consider pulmonary artery catheter to optimize preload

(PCWP).

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.

11.10

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.

11.11

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).

11.12

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.

Systemic inflammation induced by severe injury often

results in catabolism and protein wasting, making early

nutritional support imperative.

Nutrition should commence within 24-48 hours of injury.

Enteral feedings are superior to parenteral nutrition (TPN),

offering a lower infection rate and shorter ICU stays.

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.

Nutrition should include a balanced electrolyte solution

containing supplemental potassium, calcium, magnesium,

phosphate, multivitamins and trace elements (zinc, copper,

manganese, and chromium).

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.

11.13

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

11.14

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.

11.15

Chapter 12

Damage Control Surgery

Introduction

The traditional approach to combat injury care is surgical

exploration with definitive repair of all injuries. This approach

is successful when there are a limited number of injuries.

Prolonged operative times and persistent bleeding lead to the

lethal triad of coagulopathy, acidosis, and hypothermia,

resulting in a mortality of 90%.

Damage control is defined as the rapid initial control of

hemorrhage and contamination, temporary closure,

resuscitation to normal physiology in the ICU, and

subsequent re-exploration and definitive repair. This

approach reduces mortality to 50% in some civilian

settings.

What might increase the life and limb salvage rate in troops

in the field setting is the application of the damage control

concepts described above in patients with favorable

physiology.

Tactical Abbreviated Surgical Control (TASC).

ο Damage control techniques in a tactical environment.

ο Abbreviated, focused operative interventions for peripheral

vascular injuries, extensive bone and soft tissue injuries,

and thoracoabdominal penetrations in patients expected

to survive, instead of definitive surgery for every casualty.

ο This may conserve precious resources, such as time,

operating table space, and blood.

This TASC philosophy relies on further definitive surgical

care at the next echelon of care.

12.1

Emergency War Surgery

Damage control techniques should be considered in all multi-

system casualties at the onset of surgical therapy. When initially

rejected, reconsideration should occur when unexpected

findings are discovered or natural breaks in the surgical therapy

occur, following an initial decision to perform a definitive repair.

The goal of damage control is to restore normal physiology

rather than normal anatomy. It is used for the multiple injured

casualty with combinations of abdominal, vascular, genitou-

rinary, neurologic, orthopedic, and/or thoracic injury in three

separate and distinct phases:

1. Primary Operation and Hemorrhage Control - surgical

control of hemorrhage and removal of contamination;

laparotomy terminated, abdomen packed and temporary

closure; definitive repair is deferred.

2. Critical Care Considerations - normal physiology restored

in ICU by core rewarming, correction of coagulopathy, and

hemodynamic normalization.

3. Planned Reoperation - re-exploration to complete the

definitive surgical management or evacuation.

General Considerations

Philosophy of damage control is “a live patient above all else.”

ο Avoid hypothermia.

ο Rapidly achieve hemostasis.

ο Perform only essential bowel resections.

ο Close or divert all hollow viscus injuries, only performing

reconstruction at the second operation after the patient has

stabilized and can tolerate a prolonged operation.

When to employ damage control.

ο Use damage control in patients who are present with or at

risk for developing:

♦ Multiple life-threatening injuries.

♦ Acidosis (pH < 7.2).

♦ Hypothermia (temp < 34°C).

♦ Hypotension and shock on presentation.

♦ Combined hollow viscus and vascular or vascularized

organ injury.

♦ Coagulopathy (PT > 19 sec and/or PTT > 60 sec).

12.2

Damage Control Surgery

♦ Mass casualty situation.

ο Take into account ability to control hemorrhage, severity

of liver injury, and associated injuries.

ο Pack before massive blood loss (10-15 units of pRBCs) has

occurred.

ο Injuries that typically require damage control techniques.

♦ Upper abdominal injuries that are not isolated spleen

injuries (duodenal, large liver injuries, pancreas, and

so forth).

♦ Major penetrating pelvic trauma of more than one

system.

♦ Any retroperitoneal vascular injury.

To reiterate, damage control is practiced in three phases:

1. Primary operation and hemorrhage control.

2. Critical care resuscitation.

3. Planned reoperation.

Phase 1: Primary Operation and Hemorrhage Control

Phase 1 of damage control includes 5 distinct steps:

1. Control of hemorrhage.

2. Exploration to determine extent of injury.

3. Control of contamination.

4. Therapeutic packing.

5. Abdominal closure.

Control of hemorrhage/Vascular injury repair.

ο Control of hemorrhage is best done with ligation, shunting,

or repair of injured vessels as they are encountered.

ο The primary goal is hemorrhage control, not maintenance

of blood flow.

ο For the patient in extremis, clamping or shunting of major

vessels is recommended over repair.

♦ THINK: ligate/shunt ⇒ fasciotomy.

ο Additional methods of hemorrhage control include balloon

catheter tamponade of vascular or solid viscus injuries.

Exploration to determine extent of injury.

ο Damage control laparotomy.

♦ Rapidly achieve hemostasis.

12.3

Emergency War Surgery

♦ Perform only essential resections or pack solid organs

to diminish blood loss.

♦ Close or divert all hollow viscus injuries.

♦ Rapidly terminate the procedure to correct hypo-

volemia, hypothermia, and acidosis to prevent

coagulopathy.

♦ Perform definitive reconstruction only after the patient

has stabilized and can tolerate a prolonged operation.

Control of Contamination.

Contamination control also proceeds as injuries are

encountered, utilizing clamps, primary repair or resection

without reanastomosis.

With multiple enterotomies, if the area of injury represents

less than 50% of the length of the small bowel, a single

resection can be undertaken.

At this stage of the operation, the surgeon must decide

whether or not to proceed with definitive repair of the

identified and controlled injuries. Careful communication

with the anesthesiologist is critical to this decision.

♦ If aggressive resuscitation has been successful in

maintaining normal temperature, coagulation, and acid

base status, then definitive repair may proceed.

♦ If any of these interrelated factors are abnormal, the

procedure should be terminated (contamination

controlled without reanastomosis) and the patient taken

to the ICU for further resuscitation.

♦ The presence and status of extra-abdominal injuries

needs to be taken into consideration when deciding how

much physiologic reserve the patient has left.

Therapeutic Packing.

ο Resuscitative vs Therapeutic Packing.

♦ Resuscitative packing is manual compression of the

bleeding site as an initial measure in controlling or

minimizing blood loss.

♦ Therapeutic packing provides long-term tamponade of

liver, pelvic, and retroperitoneal bleeding.

ο Do not use the “pack and peek” technique wherein the

liver is packed and the patient resuscitated; the packs are

removed to identify the source of bleeding, but rebleeding

12.4

Emergency War Surgery (2004) - page 4