Snake Bites

Coral snake bites are relatively rare but potentially serious envenomations caused by the bites of venomous coral snakes, belonging to the Elapidae family. The most prevalent coral snake species in North America is the Eastern Coral Snake (Micrurus fulvius). They are the classic “red touch yellow, kill a fellow.” Here is a summary of key aspects related to coral snake bites:

Mechanism of Toxin: Coral snake venom primarily consists of neurotoxins that affect the nervous system. These neurotoxins which include micrurotoxin and micruroidin, target the neuromuscular junction at acetylcholine receptors, to which they inhibit. This can lead to respiratory depression.

Clinical Features of Coral Snake Bites:

  1. Local Symptoms: Coral snake bites often do not cause significant local symptoms, such as pain or swelling, unlike many other venomous snake bites.

  2. Neurological Symptoms: The primary clinical manifestation is neurotoxicity, characterized by weakness, difficulty swallowing, slurred speech, and respiratory failure. Patients can develop cranial nerve palsies.

  3. Respiratory Distress: Resulting from respiratory muscle paralysis. This is the primary concern after a coral snake bite.

Evaluation and Lab Abnormalities:

  1. Clinical Assessment: Diagnosis is primarily clinical, based on the characteristic neurological symptoms and a history of coral snake bite.

  2. Laboratory Tests: Laboratory abnormalities may include an elevated creatine kinase (CK) level due to muscle breakdown, reflecting the neurotoxic effects of the venom.

  3. Coagulation Studies: Unlike some other venomous snake bites, coral snake envenomation usually does not cause coagulopathy. There are rare reported cases of DIC in coral snake bites, and given that patients may not remember the type of snake that bit them, it is not unreasonable to send DIC labs.

Medical Management:

  1. Supportive Care: Normal wound care, clean the wound, update tetanus, watch for cellulitis. Do not attempt to “suck out” the venom. No indication for using a tourniquet. Extremities should be monitored for compartment syndrome.

  2. Antivenom: The only specific treatment for coral snake envenomation is the administration of coral snake antivenom (Micrurus fulvius antivenom). However, this has been out of production and current stock is expected to end this year.

  3. Ventilatory Support: Patients with respiratory failure may require mechanical ventilation until the effects of the venom wear off. This should be handled aggressively. If the patient shows any signs of respiratory failure, promptly intubate them.

It's important to note that coral snake bites are uncommon, and the severity of envenomation can vary. These patients often require admission for monitoring.

 

Crotaline bites, commonly referred to as snakebites from pit vipers such as rattlesnakes, copperheads, and cottonmouths, are the other clinically significant snakes in NA. Here's a summary covering the mechanism of toxin, clinical features, evaluation, and medical management:

Mechanism of Toxin: Crotaline venom primarily consists of enzymes and peptides that exert cytotoxic, hemotoxic, and proteolytic effects. Metalloproteinases and serine proteinases in the venom contribute to swelling and damage to capillaries. They also lead to coagulation abnormalities. 

Clinical Features of Crotaline Bites:

1.       Local Effects: Immediate pain, swelling, and ecchymosis at the bite site. Local tissue necrosis may occur, especially with rattlesnake bites.

 

2.       Systemic Effects: Hematologic abnormalities, such as thrombocytopenia and coagulopathy, due to venom-induced consumption coagulopathy. Systemic symptoms like nausea, vomiting, weakness, dizziness, and diaphoresis also occur. Severe envenomation can lead to shock, respiratory distress, and organ failure.

Evaluation, Including Lab Abnormalities:

1.       Clinical Assessment: Assess local and systemic signs of envenomation. Evaluate for signs of compartment syndrome in the affected limb. Patients can develop hypotension from significant third spacing.

 

2.       Laboratory Studies: Complete blood count (CBC) to assess for thrombocytopenia and coagulopathy. Coagulation studies, including prothrombin time (PT), activated partial thromboplastin time (aPTT), and fibrinogen levels. Blood chemistry to assess organ function.

Medical Management:

1.       Supportive Care: Normal wound care, clean the wound, update tetanus, watch for cellulitis. Do not attempt to “suck out” the venom. No indication for using a tourniquet. Extremities should be monitored for compartment syndrome. Limbs should be measured. Patients should receive IVF and may need pressors.

 

2.       Respiratory support: Patients with bites to the head and neck are at risk for airway compromise due to edema. Early intubation should be considered in these patients.

 

3.       Antivenom Therapy: There are two antivenoms approved, Crofab and Anavip. Crofab is the original, Anavip was just approved in 2015.

    1. Criteria for administration of Crofab or Anavip– significant progression of swelling, abnormal test results (plt less than 100k or fibrinogen less than 100), altered vital signs or altered mental status.

    2. Crofab is given as 6 vials, usually diluted into 1 L of NS and run over an hour. Repeat doses (2 vials) may be given if symptoms persist at 6, 12, and 18 hours. Patients should be monitored for allergic reactions.

    3. Anavip is a newer antivenom. It is given as 10 vials, repeated Q1H PRN for initial control of local signs of envenomation. 4 vials are given as maintenance for symptom recurrence.

Both antivenoms are quite expensive. Crofab is $3400 per vial and Anavip is $1200 a vial. Patients with systemic symptoms and receiving antivenom should go to the ICU.

Buchanan JT, Thurman J. Crotalidae Envenomation. [Updated 2022 Oct 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551615/

Hessel MM, McAninch SA. Coral Snake Toxicity. [Updated 2023 Mar 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519031/


Spider Bites

The brown recluse spider, scientifically known as Loxosceles reclusa, is known for its venomous bite. This spider is found in southern US states.

  1. Mechanism of Toxin: Sphingomyelinase D causes hemolysis and complement mediated erythrocyte destruction. There are multiple proteases that break down collagen, elastin, fibrinogen, etc and act synergistically with sphingomyelinase D to cause local tissue destruction

  2. Clinical Features of Bites:

    • Course of bite: The bite is often painless or with minimal pain. There will be two small puncture wounds. This will become pale with the edges becoming red. Over the next few days, this turns into a blister with a central ulcer, followed by skin sloughing. Can take weeks for wound to heal.

    • Early Symptoms (2-8 hours):

      • Redness and swelling around the bite site

      • Mild to moderate pain and itching

    • Delayed Symptoms (12-36 hours):

      • Necrotic (dead) tissue formation, leading to an ulcer

      • Systemic symptoms like fever, chills, malaise, headache, nausea

    • Worsening complications:

      • DIC

      • Rhabdo

      • Kidney Failure

  3. Evaluation: Lab tests should only be ordered in patients with systemic symptoms and fear of worsening complications. Should order CBC, CMP, CK, retic count, haptoglobin, LDH, PT/INR, D-dimer, fibrinogen.

  4. Medical Management:

    • Local Wound Care: Primary management is local wound care. Clean the site with soap and water, apply a cold compress to reduce swelling, and elevated the affected site. Sphingomyelinase D also has reduced activity in lower temp, so ice packs are important! Patient should also receive tetanus prophylaxis!

    • Pain Management: NSAIDs

    • Wound Care for Necrotic Tissue: If wound is severe enough, may require eval for debridement and potential skin grafting (this is usually weeks later). Hyperbaric oxygen therapy can also be considered for severe cases.

    • Antibiotics: Only if concern for local cellulitis.

    • Systemic Treatments: Weak evidence for use of dapsone. There is slightly more evidence behind the use of corticosteroids for reducing the risk of AKI and rhabdo.

It's crucial to note that brown recluse spider bites are rare, and most cases resolve with local wound care.

 

Black widow spiders, known as Lactrodectus spp, are venomous arachnids found in various regions around the world. The venom they produce contains neurotoxins, primarily alpha-latrotoxin, which affects the nervous system. These spiders classically have the “red hourglass” marking on them.

1.       Mechanism of Toxin: The primary toxin in black widow spider venom is alpha-latrotoxin. It works by binding presynaptic neurons, creating calcium permeable channels in the lipid layers, causing an influx of calcium into the presynaptic cells. This leads to an excessive release of neurotransmitters. Primarily concerned with release of acetylcholine.

 

2.       Clinical Features of Bites:

  • Course of bite: Bites are often initially characterized by severe local pain at the bite site. Very quickly patients will develop erythema and edema at site of bite

  • Systemic Symptoms: As the venom spreads, systemic symptoms may develop, including muscle pain and cramps, abdominal pain, weakness, sweating, and nausea. Patients may experience autonomic nervous system effects such as increased blood pressure and heart rate.

  • Worsening complications

    • Rhabdo

    • Myocarditis

    • A-fib

3.     Laboratory Tests: Lab values are generally nonspecific for black widow bites. Patients will tend to have elevated WBC, hematuria, and elevated liver enzymes. There are documented cases of rhabo and myocarditis from black widow bites, and there for kidney function and troponins can be checked if patients complain of systemic symptoms.

4.       Medical Management:

  • Local Wound Care: Clean the site with soap and water. Patient should also receive tetanus prophylaxis!

  • Pain Control: Analgesics, such as opioids or muscle relaxants, may be used to manage pain.

  • Antivenom: In severe cases or when systemic symptoms are significant, antivenom may be administered. This can rapidly reverse the effects of the venom. It is horse derived, and may cause anaphylaxis.

  • Observation: Patients may be observed for several hours to ensure symptoms do not worsen and to monitor for potential complications. Consider admission in children, patients with preexisting cardiac conditions, pregnant women, or for severe symptoms.

    It's important to note that while black widow spider bites can be painful and cause distressing symptoms, fatalities are rare.

     

    Anoka IA, Robb EL, Baker MB. Brown Recluse Spider Toxicity. [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537045/

    Williams M, Sehgal N, Nappe TM. Black Widow Spider Toxicity. [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499987/

     


Hypothermia

Hypothermia is a medical emergency characterized by a core body temperature below the normal range of 95°F (35°C).

Causes of Hypothermia:

  1. Increased heat loss

    • Homeless population

    • Elderly patients

    • Submersion injuries

    • Drugs, EtOH, CO poisoning can all cause increased vasodilation, leading to increased heat loss

  2. Decreased heat production

    • Endocrine (hypothyroidism, hypoadrenalism, hypoglycemia)

    • Erythrodermas (psoriasis, exfoliative dermatitis, eczema, burns)

    • Impaired shivering

    • Impaired thermoregulation

    • Sepsis

Swiss Hypothermia Staging System:

Stage 1: Mild (32-35°C) - Shivering, mild confusion, awake

Stage 2: Moderate (28-32°C) - Severe shivering, altered mental status

Stage 3: Severe (20-28°C) - Loss of consciousness, bradycardia, shivering may cease

Stage 4: Profound (<20°C) – Unobtainable vital signs

Associated Complications:

  1. Cardiac dysfunction

    1. Dysrhythmias can occur when body temperature drops below 30°C

    2. There is typically a drop in temperature and MAP after rewarming is started due to vasoconstriction

  2. Cold injuries (frostbite, etc. Maybe there will be more on this at a later date)

  3. Coagulopathy (patient may be coagulopathic despite normal labs because the lab rewarms the sample)

    1. Impaired clotting function

    2. Thromboembolism (due to hemoconcentration and poor circulation)

    3. DIC

  4. Impaired pharmacology

    1. Protein binding increases when temperature drops, rendering drugs ineffective

    2. Oral meds are not absorbed well due to decreased GI motility

    3. IM route is impaired due to vasoconstriction

  5. Rhabdomyolysis

General Management:

  1. Airway, Breathing, Circulation (ABCs)

    • Hypothermia causes a leftward shift in oxygen curve so support with oxygen, and prepare for intubation depending on how profound the hypothermia is

  2. ECG Findings

    • Patients usually have sinus bradycardia, can progress to a fib with slow ventricular response

    • Severe cases can develop v fib

    • Osborn or "J" waves (associated with moderate to severe hypothermia)

  3. Remove Wet Clothing - Prevent further heat loss

  4. Passive External Rewarming - Insulate the patient, provide warm blankets

  5. Active External Rewarming (should be done for moderate hypothermia)

    • Use forced warm air blankets or radiant heaters – our ED uses the Bair Hugger

  6. Active Internal Rewarming (for severe hypothermia)

    • Warmed intravenous fluids (warmed to 38-42°C)

    • Heated humidified oxygen

    • Various lavages (Thoracic, peritoneal, bladder, GI)

Management during Cardiac Arrest:

  1. CPR – initiate if patient does not have a pulse (should also assess if patient is still breathing)

    • It is challenging to assess vital signs in hypothermic patients - use end tidal or POCUS to help assist to see if patient is breathing and has cardiac function

    • Starting CPR if the patient does have a pulse may precipitate ventricular rhythms

    • Hypothermic patients have higher chances of improved neurological outcome and survival than normothermic patients that arrest

  2. Defibrillation

    • Use defibrillation if indicated, but note that hypothermic patients may not respond to defibrillation until adequately warmed

  3. ECMO

    • Patients with refractory hypothermia should be considered for ECMO

    • Patients with out-of-hospital-cardiac-arrest that are hypothermic should ideally be transported to an ECMO center

    • If patient is unstable (dysrhythmia, severe hypothermia, etc) ECMO teams should be contacted early in the ED visit

 

Stay warm out there this weekend!

 

Paal P, Pasquier M, Darocha T, Lechner R, Kosinski S, Wallner B, Zafren K, Brugger H. Accidental Hypothermia: 2021 Update. Int J Environ Res Public Health. 2022 Jan 3;19(1):501. doi: 10.3390/ijerph19010501. PMID: 35010760; PMCID: PMC8744717.

Baumgartner EA, Belson M, Rubin C, Patel M. Hypothermia and other cold-related morbidity emergency department visits: United States, 1995-2004. Wilderness Environ Med 2008;19:233-237

Brown et al., Accidental Hypothermia. N Engl J Med 2012; 367:1930-1938