Scuba Emergencies (ascent)

Scuba Diving Emergencies (Ascent)

*rare, but commonly tested topic! 

*includes sinus barotrauma, “face squeeze,” pulmonary barotrauma, decompression sickness, arterial gas embolism, nitrogen narcosis, oxygen toxicity, carbon monoxide toxicity, hypothermia, and even caustic injuries.

*today’s POTD will primarily focus on barotrauma of ascent

Decompression Sickness

·       aka “the bends”

·       Mostly after rapid ascent from diving;  less commonly following high altitude aviation ascent and hypobaric training

·       Onset

•   symptom onset ~ 6 hours after surfacing, but as quickly as 10 minutes after

·       Pathophysiology

• Results from the expansion of inert gas (nitrogen>helium) that dissolved in tissues during descent

  • As the pressure of these gases exceeds atmospheric pressure, they bubble and lodge in veins leading to localized venous obstruction and inflammatory cascades

·       Types

•   Type I

  • Less dangerous

  • Constitutional symptoms

  • Joint/extremity involvement/pain

    • Shoulder, elbow, knee

  • Skin/lymphatic involvement

    • Pruritis, paresthesias, hot/cold disturbances, pittng edema

    • “Scarletiniform” rash secondary to nitrogen passage through sweat glands

    • “Cutis marmorata” marbling purple/blue discoloration  

• Type II

  • Multiple joint involvement

  • Spinal cord involvement

    • Ascending paralysis/paraesthesias

    • Urinary retention, fecal incontinence, priapis

  • Vestibular involvement

    • Vertigo, tinnitus, hearing loss

  • Pulmonary involvement

    •   Cough, chest pain, sob, hemoptysis

• Type III

  •   Type II + Arterial Gas Embolism (see below)

  • Essentially stroke symptoms

·       Work up and Management

• Clinical diagnosis

•   BGM, full set of labs (cbc, bmp, lfts, pt/ptt, vbg, etoh)

• Supine, not trendelenberg

• IVF

•   “De-nitrogenation” with 100% NRB, to be continued 2 hours after symptom resolution

•    Hyperbaric therapy for Type II and III

  •   If need to transport, then preferably ground and not air  

Arterial Gas Embolism

·       Can occur after diving, dialysis, pregnancy, etc.

·       Onset

• AGE from scuba diving occurs during ascent or immediately after

·       Pathophysiology

• Rapid ascent without exhalation leading to lung volume expansion, alveolar rupture, and gas leakage (air or nitrogen) into the pulmonary veinsàleft heartà systemic circulation

  • Can embolize to different parts of the brain, often cerebral arteries

·       Symptoms

• Suspect in anyone who’s lost consciousness on ascent or within 10 min of surfacing

  • But symptoms can vary depending on location of embolization (see below)

    • Coronary

      • Dysrhythmia, MI, cardiac arrest

    • Cerebral

      •   Stroke symptoms, visual deficits, seizures

    •    MSK

      • Cyanosis

    •   Renal

      •   Hematuria, proteinuria, ARF

·       Work up and Management

•    Labs as above

•   TEE if available

•   Supine

•    IVF

•   100% NRB while transporting to hyperbaric facility, intubate if necessary

Post-Intubation Hypotension

Post Intubation Hypotension

*you intubated someone and they just became hypotensive. Is there more to consider than RSI taking away their inherent sympathetic drive? Think of the “AAHH SHITE” mnemonic the next time you’re in this stressful situation.

Acidosis

·       This pH disturbance contributes to a reduction in cardiac contractility/output and arterial vasodilatation leading to hypotension

·       Consider administering bicarb peri/post intubation (very controversial)

Anaphylais

·       Uncommon in general, but more likely to happen from neuromuscular blocking agents than ketamine/eotmidate

o   succinylcholine > rocuronium > atracurium

§  sugammadex (reversal agent for roc) unlikely to reverse the anaphylaxis

Heart: Tamponade

·       Consider in both traumatic and nontraumatic (medical) presentatoins

o   Suspect in those with history of (recent) malignancy, ESRD, and those on anticoagulation

·       These pts are very preload dependent, and by intubating/providing positive pressure ventilation (PPV) you are increasing intra-thoracic pressure thereby decreasing venous return and further declaring the obstructive process

Heart: Pulmonary Hypertension

·       PPV+hypoxia+hypercapnea further increase the pulmonary artery pressures and right ventricular pressure

o   worsens RV ischemia/overload and bowing into the LV causing decreased LV filling and eventually decreased cardiac output

·       In these patients, consider an awake intubation to decrease risk of systemic hypotension from RSI meds as well as hypercapnea secondary to an apneic episode

·       Consider ketamine without a paralytic agent as it will maintain respiratory drive

Stacked breaths/autopeep

·       Consider in those with obstructive lung pathology who have tendency of breath stacking

o   Leads to progressive air trappingà increased intra-thoracic pressureàdecreased preloadàhypotension

Hypovolemia

·       Typically in setting of sepsis and hemorrhage

o   Give a bolus of appropriate resuscitative fluid

Induction Agent

·       Decrease vascular tone and venous return

·       Consider ketamine and push dose pressors if patient already hemodynamically unstable

·       “Dose Induction Agents Low and Paralytic Agents High”

·       Consider awake intubation

o   Helps maintain their endogenous catecholamines

Tension PNX

·       Endotracheal intubation carries the risk of barotrauma manifesting as a (tension) PNX

·       Perform a chest US or CXR if unsure

·       Perform a needle/finger thoracostomy if necessary

Electrolytes

·       Consider electrolyte derangement(s) such as hyperkalemia if certain medications (succinylcholine) administered and the patient develops a dysrhythmia  

emDocs

rebelEM II

rebelEM III

REBOA

REBOA or Resuscitative Endovascular Balloon Occlusion of the Aorta

click here for brief visualization

Background

• Leading cause of preventable trauma related death is hemorrhage

  • more specifically, non-compressible hemorrhage--the type we cannot see or stop with direct pressure, tourniquets, pressure devises.

    • examples include solid organs bleeding into the chest and abdomen as well as large vessel bleeding

• For major penetrating/blunt injuries causing traumatic arrests and hemorrhagic shock states, proximal aortic control ("cross clamping" the aorta) to stop forward flow into the abdominal aorta is key

  • traditional approach is via the left anterior thoracotomy

  • at the discretion of the ED/trauma teams, REBOAs are now being used as the relatively minimally invasive approach to clamping the aorta and thus increasing afterload and obtaining control of noncompressible hemorrhage below the diaphragm (see below)

    • prior to this, the REBOA was mainly used for the management of ruptured AAAs in the 2000s

Technical aspects

·       Femoral artery access (percutaneous or via a cut down) 

·       Seldinger's technique to advance the balloon over a wire and to the desired location

·       The intra-aortic balloon can be placed at different levels (aka "ZONES") to provide the appropriate occlusion for the likely injury at hand

·       XR confirmation of catheter/balloon at desired location is necessary prior to inflation (see below)

Zones 

·       Zone I 

o   Left subclavian artery to celiac artery (above the diaphragm)

o   Occluded for intra-abdominal hemorrhage (positive FAST)

o   CXR to visualize balloon above the diaphragm (at level of ~xiphoid)

   Zone II

o   Celiac artery to renal artery (around the diaphragm)

o   NO OCCLUSION ZONE

Zone III

o   Lowest renal artery to aortic bifurcation (infrarenal aorta)

o   Occluded for pelvic hemorrhage likely from pelvic fracture or iliac/common femoral vascular compromise (negative FAST)

o   Pelvis XR to visualize balloon below the diaphragm at approximately the level of L2 or L3 (at level of ~umbilicus)

Limitations and Complications

·       Contraindicated in thoracic injuries

o   Ideally need a CXR prior to insertion to evaluate for other intra-thoracic/aortic injury

·       Balloon over-inflation can cause aortic rupture

·       Need to immediately proceed to the OR for ex-lap or angio-embolization

o   Within OR, can keep balloon inflated for up to 60 min

·       12F sheaths as opposed to smaller 7F ones require removal via open femoral cut down and repair of arteriotomy site, which in itself is very risky

·       Not enough large center studies to fully support it yet

In Summary:

LITFL

https://www.youtube.com/watch?v=W8yGPeGkuJg

Resuscitative endovascular balloon occlusion of the aorta: current evidence