Special Operations Forces Medical Handbook

4-24

Plan:
Treatment
Primary:

1. Prevent PE in high-risk post-op patients by frequent and early ambulation; use of 5000 U heparin IV or
   SC (low-molecular weight heparin) every 8-12 hours; external pneumatic compression, and gradient elastic
   stockings.


2. Evacuate patients with PE and those with risk factors and suspicion of PE.


3. If the risk of bleeding is low, use heparin as above while en route or awaiting evacuation with severe PE.


4. Administer oxygen 2L via nasal cannula. Use mask and increased rate in massive PE.


5. Administer IV uids (see Shock: Fluid Resuscitation) to help maintain cardiac function in massive PE.

Patient Education
General: Avoid thrombus in high-risk patients.
Activity: Early ambulation to avoid PE. No activity during PE until anticoagulated at referral facility.
Medications: Avoid anticoagulants such as aspirin or NSAIDs while on heparin to minimize bleeding risks.
Prevention: Avoid lower extremity activity or intra-abdominal strain that could dislodge additional thrombus
if already have PE. Maintain blood ow during prolonged travel or bedrest by walking and stretching to
avoid PE.

Follow-up Actions
Evacuation/Consultation Criteria: Emergently evacuate patients with PE, and those with risk factors and
suspicion of PE. Consult pulmonologist or internist.

Respiratory: Acute Respiratory Distress Syndrome

COL Warren Whitlock, MC, USA

Introduction: Acute Respiratory Distress Syndrome (ARDS - was previously Adult Respiratory Distress
Syndrome) can result from either direct trauma to the lung (infection, pulmonary contusion, aspiration, inhala-
tion of toxic substances – including nitrogen mustard) or secondary to systemic pathology, such as shock or
septicemia, which causes serous uid from the blood stream to “leak” into the lungs. ARDS is characterized by
a sequence of events, beginning with diffuse pulmonary edema, that are now thought to be part of an inam-
matory cascade that causes multiple organ failures. The pulmonary edema resembles diffuse pneumonia or
congestive heart failure on CXR but is not directly due to heart failure. ARDS is sometimes referred to as
non-cardiac pulmonary edema, wet lung syndrome, or Da Nang lung (seen in Vietnam War). Renal failure,
diffuse intravascular coagulation (DIC) or liver failure may precede or follow lung failure. ARDS cases rapidly
deteriorate and die (100% mortality) without ICU and ventilatory support. Mortality is 50% even with such care.
There are 4 recognized phases:
Phase 1: Acute injury: Normal physical exam, normal chest x-ray, tachypnea, tachycardia and respiratory
alkalosis (low CO 2 partial pressure and high blood ph)
Phase 2: Latent phase (6-48 hours after injury): Hyperventilation, hypocapnia (low CO 2 ), increase in
work of breathing, hypoxemia
Phase 3: Acute respiratory failure (48-96 hours after injury): decreased lung compliance, diffuse infiltrates
on CXR due to pulmonary edema
Phase 4: Multi-organ failure: Severe hypoxemia unresponsive to therapy, metabolic and respiratory
acidosis (high CO 2 partial pressure and low blood ph)

Subjective: Symptoms
See phases above. Difficulty breathing and severe shortness of breath, rapid progression (2-24 hours) of
respiratory failure, increased agitation.
Focused History: (Patient may be too ill to provide comprehensive information.) Duration: How long ago did
you start feeling sick? (ARDS usually begins 24-48 hours after the initial insult i.e., septic shock.) Alleviating
or Aggravating Factors: Did symptoms get better then worse? (In some cases symptoms seem to be
improving, then worsen— like appendicitis, which wanes after rupture then progresses to septic shock.)