Environmental Emergencies

Environmental Emergencies
National Resident Review Course Ian Rigby

Outline What’s New in Environmental Emergencies? Diving Emergencies
High Altitude Illness Snakes Spiders On the downloadable presentation is presentation notes for Heat Illnesses and Cold Illnesses - under Presentations

What’s New? Not much! These topics are admirably covered in standard text books and very little is groundbreaking since they’ve been written. Great reference is EMCNA May 2004

What’s New? Cochrane Protocol for “Recompression and adjunctive therapy for decompression illness” Recompression therapy is standard for the treatment of DCI, but there is no randomized controlled trial evidence. Both the addition of an NSAID or the use of heliox may reduce the number of recompressions required, but neither improves the odds of recovery. The application of either of these strategies may be justified. The modest number of patients studied demands a cautious interpretation. Benefits may be largely economic and an economic analysis should be undertaken. There is a case for large randomized trials of high methodological rigour in order to define any benefit from the use of different breathing gases and pressure profiles during recompression therapy.

Diving Injuries

Gas Laws Boyle’s Law Dalton’s Law Henry’s Law

Gas Laws – Boyle’s Law PV=k @ constant temp
For every 10m of depth you increase pressure by 1 atm So the size of bubbles in solution increases as pressure decreases That’s why bubbles are small at the bottom of the glass and get bigger at the top

Dalton’s Law What is (Daltin) in the beer bubbles.
The pressure of a gas is the sum of the partial pressures of all it’s gasses Pair = PPO2 + PPN2 + PPCO2 …etc Let’s assume 20% 02 and 80%N2 in air At 1 atm of air (i.e. sea level) you are inspiring 0.2 atm pressure of O2 and 0.8 atm of N2

Dalton’s Law At 30m depth (underwater) you are being subjected to 4 atm of pressure Now breathing compressed air at 4 atm (20% O2 and 80% N2) Pair = PO2 + PN2 At 4atm you are getting 0.8atm O2 and 3.2 atm of N2 So, at depth you are breathing in more molecules of the gasses

Henry’s Law The number of beer bubbles
The amount of any given gas that will dissolve in a liquid at a given temperature is a function of the partial pressure of that gas in contact with the liquid The higher the pressure, the more gas is dissolved in the solution

So…. If Dalton’s Law means we are inhaling more of a gas with increasing pressure and…. Henry’s law says with increased pressure, more gas dissolves into a liquid and… Our tissues (muscle, nerves, blood) are mostly liquid then…. As pressure increases more gas is dissolved into our tissues We’ll see how this works out in a bit

External Ear Barotrauma
Diving Emergencies Diving Emergencies Disorders of Decent External Ear Barotrauma Middle Ear Barotrauma Inner Ear Barotrauma Facial Barotrauma Sinus Barotrauma Disorders at Depth Oxygen Toxicity Nitrogen Narcosis Hypothermia Disorders of Ascent Acute Gas Embolism Pulm Hemorrhage Alternobaric Vertigo Rapid Ascent Barodentalgia Pneumo’s Long/Deep Dive DCS II DCS I Key Question in Hx

Descent – Facial Barotrauma
Failure to equalize pressure in mask Leads to traction on face, eyes due to relative negative pressure See edema and petechial hemorrhages of skin, sclera

Middle Ear Barotrauma Failure to equalize pressures of eustasian tube and the outer ear canal Leads to squeeze on the TM Most common disorder of diving

Middle Ear Barotrauma Various grades of injury of TM
1 – Capilary dilation 2 – Mucosal edema 3 – Hemorrhage into TM 4 – Hemorrhage or serrous exudate 5 – TM rupture Treat conservatively

External Ear Barotrauma
Due to plug of the external canal with a patent eustachian tube Develops a relative negative external pressure and bowing of the TM outwards

Inner Ear Barotrauma Rare
Occurs with rapid pressurization of the inner ear leads to a pressure wave that disrupts the cochlear round window Presents with sensorineural hearing loss and severe vertigo Usually requires ENT f/u Can test by using insufflator in the ear – increasing and decreasing pressure induces nystagmus

Sinus Barotrauma Same theory with the ear can lead to sinus pain either in descent or ascent if the sinuses fail to equalize pressure Treat with pseudophed or other OTC decongestants

Injuries at Depth Nitrogen Narcosis Hypothermia Oxygen Toxicity

Nitrogen Narcosis Rapture of the Deep Dalton’s law says….
At depth inspiring more N2 Henry’s law says…. More N2 diffusing into tissues

Nitrogen Narcosis Nitrogen has a special affinity for fatty tissue
Diffuses into neural membranes and acts like an anesthetic gas Causes euphoria, poor judgment and impaired motor skills Injury occurs due to lack of judgment Treatment is ascent

DCS – Decompression Sickness

DCS I – ‘the bends’ Occurs with ascent from depth
Especially with long times at depth Presents with periarticular joint pain Can also see skin itching and marbling in DCS I Occurs when N2 forms bubbles in tissues Leads to obstructive and inflammatory changes DCS is more than just bubbles Is DCS I if symptoms limited to MSK system only Relief when joint compressed with BP cuff at 200mmHg

DCS I – Treatment Treat by recompression therapy (hyperbaric O2)
Can utilize 100% O2 Search for DCS II symptoms….

DCS II Decompression sickness involving anything more than the MSK system Treatment for all is supportive care and recompression therapy (hyperbaric) So what is DCS 2?

DCS II - CNS CNS – nitrogen dissolves easily into the fatty myelinated tissues of the nervous system So has predilection for formation of bubbles with decompression Spinal cord findings common especially in the thoracolumbar area Presents as paresthesias, weakness, etc. Can present as CVA Inner Ear DCS gives vertigo – ‘the staggers’ LOC is uncommon (as opposed to AGE)

DCS II – ‘the chokes’ Pulmonary circulation is a low pressure system
Large volume/size bubbles can cause venous gas emboli Get progressive cough, chest pain, dyspnea in the 1st 24hr of surfacing What gas laws? Tx with supportive care, 100% O2 & recompression So as lungs are low pressure system how does boyle’s law come into play (PV=k)

Rapid Ascent–Acute Gas Embolism
2nd leading cause of death in diving Rapid ascent causes bubble formation in pulmonary circulation These can traverse the L atrium and ventricle and are sent to the systemic circulation 60% of those who suffer AGE have demonstrated right to left shunts (i.e. patent foramen ovale, etc.) Bubbles cause mechanical obstruction and then inflammatory rxn Onset of symptoms occurs within 10min of surfacing (90% of the time)

AGE – CNS/CVS Predilection for cerebral and cardiovascular circulation
Altered LOC Seizures Visual changes CN deficits Focal weakness Predilection for cerebral and cardiovascular circulation Ischemia MI Dysrhythmias These are really tissue that do not function well with obstructed circulation

AGE - Treatment Supportive care 100% O2
Recompression therapy (only definitive tx)

Pneumothorax Occurs with alveolar damage and gas crossing the visceral pleura Treat as standard pneumo Needs chest tube (not just aspiration) if patient undergoing recompression tx

Pneumomediastinum Air bubbles dissecting into pulmonary interstitium
Goes into neck, pericardium, mediastinum Unless hemodynamically unstable, treat conservatively and gas will absorb on own

Alternobaric Vertigo Rare
Failure to equalize pressure of the inner ear on ascent. Occurs with blockage of unilateral eustacian tube Develops pressure difference from middle ear and cochlear organ Get profound vertigo, nausea Once pressures equalize symptoms disappear

Diving Comes Down to Beer Bubbles
Boyle’s Law describes size of bubbles Dalton’s Law describes what’s in the bubbles Henry’s Law describes the gas dissolved in the liquid and the number of bubbles

High Altitude Illnesses

Am I High Yet? No absolute definition for high altitude
The most accepted is altitudes greater than 2500 m Very high is m Extreme is >5500 m

Where Can I Go To Get High?
High altitude (>2500 m) is found only in western Alberta, British Columbia and the Yukon Banff 1372 m Lake Louise 1646/2637m Sunshine 1658/2729m Whistler 652/2182m Mt.Columbia 3747m Mt. Logan 5959m

More About Gas! At sea level we are underneath an ocean of air
PiO2 = 0.21(PB-47) PB=barometric pressure At sea level PiO2= 160 mm Hg  At 2500m PiO2 = 119 mm Hg  Aconquilcha,Chile 5340m PiO2 = 82 mm Hg On top of Everest (8848m) PiO2 = 43 mm Hg  At sea level we are underneath an ocean of air %O2 is always 21% But as you climb higher, the Patm drops and thus your PO2 drops So what gas law here. Dalton’s law Patm=PO2+PNO2 +PCO2

Respiratory Adaptations
Hypoxia sensed by carotid body (PaO2<60) and signals the brain for an increased respiratory rate (hypoxic ventilatory response - HVR) After 30 minutes, the resulting respiratory alkalosis is sensed in the brain stem and the medullary respiratory centre limits HVR The respiratory alkalosis is sensed by the kidney, which begins to excrete HCO3-, allowing the HVR to increase over the next week.

Circulatory Adaptations
Hypoxia stimulates increased catecholamines Thus a transient increase in cardiac output, heart rate, venous tone, and blood pressure Hypoxia signals an increased cerebral blood flow (CBF) Hypoxia causes pulmonary vasoconstriction Cardiac function returns to baseline quickly but shows a decreasing ability to generate higher cardiac output with exercise

Hematologic Changes Within 2 days of ascent plasma volume falls due to diuresis and fluid shifts causing hemoconcentration Erythropoetin is released rapidly on ascent and a few days later RBC mass increases Enough physl – onto clinical presentations

Some Definitions AMS - Acute Mountain Sickness HAPE
- High Altitude Pulmonary Edema HACE - High Altitude Cerebral Edema HAFE - High Altitude Flatus Expulsion

Acute Mountain Sickness (AMS)
Onset hours after arrival at altitude (can be 2-96 hr) Very Common 66% of Climbers on Mt. Rainier 50% of visitors to Khumbu region of Nepal 20% of visitors to Colorado ski resort

AMS Diagnosis 1991/93 Lake Louise Consensus
Recent gain in altitude Headache 2 of the following: Fatigue or weakness GI symptoms (nausea/vomiting/anorexia) Dizziness or lightheadedness Difficulty sleeping

AMS Risk Factors Higher risk populations include: Rapid altitude gain
Previous AMS Children and teenagers People taking alcohol or other respiratory depressants

What Causes AMS? Bottom line is we don’t truly know
AMS is likely due to mild cerebral edema and a generalized high sympathetic tone It is very likely that AMS/HAPE/HACE are a continuum of the same pathophysiological process

Prevention of AMS Gradual ascent beginning below 2500m
Rest on the first day above 2500m Gain no more than m per day (sleeping altitude) Two nights at same altitude every three days Avoid ETOH, sedatives, etc as they depress HVR especially at night

Prevention of AMS Acetazolamide 125 – 500 mg BID beginning 24h prior to departure and continued for 3-4d Causes a metabolic acidosis that allows for greater HVR Diuresis helps with fluid shifts Well designed trials demonstrating acetazolamide as effective in prevention

Prevention of AMS Dexamethasone 4 mg q6h Will prevent AMS
Unknown physiology but likely relieves minor cerebral edema and produces euphoria Has side effects (hyperglycemia/psychosis) Rebound common when drug stopped Generally not used in prophylaxis

Treatment of AMS Mild Symptoms
Does not need descent if mild Sx and constant supervision Stop ascent until better Acetazolamide Tylenol/ASA for Sx Consider O2 at 1-2 LPM Moderate or Unresolving AMS Descent 500 m Consider: O2 at 1-2 LPM Hyperbaric therapy Dexamethasone 4mg PO q6h until able to descend May ascend after symptoms resolve

High Altitude Pulmonary Edema

HAPE Diagnosis Recent gain in altitude 2 of the following (symptoms):
Dyspnea at rest Cough Weakness or decreased exercise performance Chest tightness or congestion 2 of the following (signs): Central cyanosis Audible rales in at least one lung field Tachypnea Tachycardia

Pathophysiology of HAPE
Radiologically demonstrates a patchy edema of the lungs This edema is protein rich and contains large amounts of inflammatory mediators Cardiac catheter studies demonstrate pulmonary hypertension with normal wedge pressures and slightly decreased cardiac output

Over Perfusion Model Nonuniform hypoxic vascular congestion in the pulmonary bed Areas with high precapillary constriction are spared This shunts excessively high pressures to areas of lesser constriction in the lungs The pressure and volume overload leads to capillary wall damage and leakage

Neurogenic Model Swelling and distortion of brain matter elicit an increased sympathetic tone and neurogenic pulmonary edema Increased sympathetic tone causes increased pulmonary arterial and venous constriction forcing edema into the lungs Some evidence that sympathetic tone also modulates the vascular permeability Few animal studies show neurogenic pulmonary edema can be stopped with adrenergic blockade - only one human study showing no effect Is neat as it attempts to link HAPE and HACE

Prevention of HAPE Gradual ascent as with all AMS
Nifedipine 20 mg TID will help prevent HAPE Unknown if acetazolamide helps prevent HAPE

Nifedipine Ca2+ channel blocker that causes vasodilation in the pulmonary system Helps reduce the hypoxic pulmonary vasoconstiction seen at altitude 2 trials demonstrating its effectiveness in preventing HAPE

Treatment of HAPE Descent Oxygen at 4-6 LPM
Nifedipine 10mg SL then 20 mg TID Hyperbaric Oxygen (i.e. Gamow Bag) PEEP

Nifedipine Ca2+ channel blocker that causes vasodilation in the pulmonary system Helps reduce the hypoxic pulmonary vasoconstiction seen at altitude 4 reasonable trials demonstrating its effectiveness in treating acute HAPE

Gamow Bag Temporizing measure to allow for descent
Using a pump creates hyperbaric pressure Places 1/8th an atm of pressure above ambient 6000m-> 3975m in bag

High Altitude Cerebral Edema

Diagnosis of HACE Recent gain in altitude In a person with AMS:
Mental status changes or Ataxia (tandem gait) In a person without AMS: Mental status changes and Ataxia

Progression of HACE Occurs in 2-3% of those trekking >5500m
Usually takes 1-3 days at altitude to develop Ataxia is usually the earliest sign May rapidly progress to coma in hours Mortality in untreated patients is 13% If progresses to coma, mortality is 60% Recovery to completely normal neurological function usually takes weeks

Pathophysiology of HACE
Vasogenic edema model CT/MRI data shows prediliction for white mater tracts Some limited animal studies support a nonuniform increased cerebral blood flow (like the HAPE model) and loss of cerebral autoregulation Human studies with doppler flow suggest that increased CBF alone is not the causative factor

Prevention of HACE Gradual ascent as per AMS
Acetazolamide thought to help (no studies) Nifedipine ineffective (1 study) Prophylactic dexamethasone not studied

Treatment of HACE Descent, descent, descent! Descent Oxygen at 2-4 LPM
Dexamethasone 4mg PO/IM/IV q6h Hyperbaric therapy

Dexamethasone Considered very helpful temporizing measure to assist in descent Thought to reduce cerebral edema CT/MRI studies have not demonstrated significant radiological decreases in edema in AMS/HACE Symptom scores in AMS/HACE are improved, and tests of neurological function do improve

To Wrap It Up Altitude illnesses are common to travelers in the rockies Prevention is key with slow accent Treat AMS with cessation of ascent, acetazolamide, oxygen, symptomatic tx. Descend if worsening Treat HAPE with descent! Consider O2, hyperbaric therapy, nifedipine and acetazolamide Treat HACE with descent. Consider O2, hyperbaric therapy and dexamethasone

Flashback! 35 yr old diver comes to see you
6 hours ago had a very long and deep dive He has now developed pleuritic chest pain (onset 1.5 hr after dive) and cough His vitals HR 80, RR14, BP 120/80 and O2Sat 98% Chest is clear to auscultate and CXR is normal

Flashback What is your DDx? What would you do to treat this person?

Altitude…Where Else?

Air Transport and the Medical Patient
All contraindications are relative Weigh risk of altitude with the benefit or rapid transport.

Altitude Trouble Open Intracranial Wounds Open Globe Injuries
ETT Cuffs Pneumomediastinum Pneumoperitoneum Pneumothorax Bowel Obstruction

Snakes! I Hate Snakes! Snakes, OK I HATE SNAKES.

North American Poisonous Snakes
Croatalids/Viperidae (Pit Vipers) Account for 98% of reported bites Elapidae (Coral Snakes)

Another Great Reason to Be Canadian!
Timber Rattler Where are the rattlers in Canada? Western Rattler Massasaga Rattler

The USA Vipers everywhere Only few coral snakes

Hey Doc! Is This Snake Poisonous?
Identifying the Pit Viper

Identifying Coral Snakes “Red on Yellow Kills a Fellow” Sonoran Coral Snake

“Red on Black, Venom Lack” Milk Snake - nonvenomous

Pathophysiology of Poison Bites
Digestive Enzymes Cause local pain, erythema, swelling, petechia, hemorrhagic blisters Hematologous Proteins Lead to coagulopathies Neurotoxins Cause muscle weakness, nerve palsies, etc. Pit Vipers Coral Snake

Pit Viper Bites 20% are dry bites (no evenomation)
Primary problem for humans is the local effect of the digestive enzymes Can also have hematological effects, seen more often in children or with direct arterial envenomation.

Field Treatment of Pit Viper Bites
Don’t get bit Immobilize the limb. Med J Aust. 1982;1: Aust Fam Phys. 1983;12: Gentle tourniquet (should be able to get 2 fingers under tourniquet) - debatable. Ann Emerg Med. 1992;21: Don’t use:cryotherapy, electric shock, arterial tourniquets, excision, or incision Joke re incision and drainage … if have a beer or two tonight.

ER Treatment of Pit Viper Bites
ABCs as usual Local wound care Draw off CBC, coags, CK, fibrinogen, Type&Hold in anticipation of potential coagulopathies Grade your evenomation and consider use of antivenom.

Grading Evenomations - N Engl J Med 2002;347(5):347–56
Minimal Envenomation Local: swelling, erythema, and/or ecchymosis confined to the site of the bite Systemic: no systemic signs or symptoms Coagulation: no coagulation abnormalities; no other significant laboratory abnormalities Moderate Evenomation (consider antivenom) Local: progression of swelling, erythema, and/or ecchymosis beyond the site of the bite Systemic: non–life-threatening signs/symptoms (nausea, vomiting, perioral paresthesias, fasciculations, mild hypotension) Coagulation: mildly abnormal coagulation profile without clinically significant bleeding; mild abnormalities on other laboratory tests Severe Envenomation (likely giving antivenom) Local: rapid swelling, erythema, and/or ecchymosis involving the entire extremity Systemic: markedly severe signs and symptoms (hypotension [systolic blood pressure <80 mmHg], altered sensorium, tachycardia, tachypnea, or respiratory distress) Coagulation: markedly abnormal coagulation profile with evidence of bleeding or threat of spontaneous hemorrhage (markedly prolonged prothrombin time, unmeasurable activated partial thromboplastin time, severe hypofibrinogenemia, severe thrombocytopenia with platelet count <20,000/mm3, and the presence of fibrin degradation products)

AntiVenoms – There are now Two!
Antivenin Crotalidae Polyvalent (ACP) (equine) Wyeth Crotalidae Polyvalent Immune Fab CroFab (Ovine) Savage Laboratories

Dosing Antivenoms ACP FabAV/CroFab Guide dosing by severity of effects
Give over 1 hour Moderate envenomations get vials of ACP Severe get 15 vials Profound circulatory collapse get 20 vials FabAV/CroFab

Notes on Antivenoms ?Which is best?
There is a high percentage of allergic rxns to both ACP and FabAV. This includes anaphylactic/anaphylactoid rxns as well as delayed serum sickness rxns Recent studies have documented a significant rebound effect in the 1st 24 hours after evenomation, so patient may require more antivenom Antivenoms work well on systemic symptoms, but poorly on local symptoms.

Local Injury

Local Injury Local wound care
Consider admission for blister management and delayed debridement Antivenom not very effective for local injury Often appears to be compartment syndrome, but most often compartmental pressures are normal, so….. DON’T LET THE SURGEONS DO FASCIOTOMY WITHOUT MEASURING COMPARTMENT PRESSURES!

Coral Snakes (Elapidae)
These guys are different than the pit vipers Their bite contains neurotoxins only, so local reactions are rarely seen (i.e. can look like a dry bite). Do not have hematological effects Neurotoxic effects can be delayed, with case reports of up to 12 hr delay

Coral Snakes EMS/First Aid is the same as for the pit vipers
Even if asymptomatic, admit for 24hrs observation For any eastern coral snake bite with possible envenomation, three to five vials of Antivenin (Micrurus fulvius) should be administered immediately. Note this is antiCoral antivenom, not ACP or FabAV! If systemic manifestations are present, at least six to 10 vials should be administered. One exception is the Arizona coral snake (Micruroides), which is not associated with human fatality and for which no antivenin exists

Review EMS – immobilize limb/2 finger tourniquet
ABCs – people survive with supportive care ? What type of snake was it ? If pit viper – grade evenomation and consider indications for antivenom 2 types of pit-viper antivenom, ACP and CroFab Don’t allow fasciotomy without compartmental pressure monitoring For coral snakes, bites may look dry Admit and consider antiCoral antivenom even if no current signs of toxicity (depends on history of snake bite)

Itsy Bitsy Spider….

Spider Stuff Most spiders are venomous, but most lack apparatus tough enough to penetrate human skin Difficult diagnosis as often spider not seen or obtained Very few deaths yet over US reported bites/yr

ED Presentations – Canadian, eh!
Local Reactions Nearly all spider bites can present like this Necrotic Arachnidism Brown Recluse, Hobo Spider in N. America Question if Wolf Spider and Jumping Spiders can cause this. Only questionable reports in South America and Australia Systemic Classically Black Widow Can occur with others too (less well described)

Culprits – Black Widow Latrodectus mactans
Only the female can envenomate humans Classically black and glossy with red abdominal markings (hourglass) Commonly found under rocks, woodpiles, etc Both local and systemic rxns

Culprits – Black Widow Worldwide distribution, including southern Canada

The Bite of the Black Widow
Black widow venom has a multitude of agents but alpha-latrotoxin is most likely culprit This acts at the presynaptic membrane of the neuronal and the neuromuscular junctions and causes the opening of nonspecific cation channels results in increased neurotransmitter release and decreased reuptake of neurotransmitter primary symptom of envenomation is muscle cramping due to release of acetylcholine at the neuromuscular junction

Bite of the Black Widow – Local Presentation
Pinprick bite In minutes get crampy pain at site Local rxn causing a flat erythematous ring 5 to 15 mm away from a central macule which fades in 12 hours (halo lesion) No local cytotoxic necrosis

Bite of the Black Widow – Systemic
Proximal muscle cramping pain begins. Pain in back, chest, or abdomen occurs depending on the anatomic location of the bite. Pain may wax and wane. Autonomic nervous system symptoms include nausea, vomiting, sweating, hypertension, tachycardia, and, rarely, priapism. These symptoms persist for 36 to 72 hours. Milder symptoms and a sensation of being “not quite right” may last for 1 to 2 weeks. Usually not life threatening unless large evenomation of small child

Black Widow Bite Treatment
Local wound care & tetanus as indicated Analgesic (often require parental opiods) Benzodiazepines as second line agents if considerable cramping symptoms (one retrospective study only) Calcium gluconate long touted as treatment, but studies do not demonstrate much success so Ca falling out of favor. Am J Trop Med Hyg 1981; 30:273–277 Ann Emerg Med 1992; 21:782–787

Black Widow Bite Treatment - Antivenom
There is a horse serum derived antivenom Indications: severe pain that is refractory to opioid analgesics life-threatening hypertension and tachycardia uncontrolled with supportive care Problems: Approximately 10% have acute allergic rxn

Culprits – Brown Recluse
Loxosceles reclusa Range from tan to dark brown Classic marking is the violin shaped dark area on the cephalothorax Have 3 pairs of eyes (most spiders with 4) 1-5cm length (leg to leg)

Culprits – Brown Recluse
Southern USA But bear in mind that can get stragglers transported. We have a documented case in Calgary

Culprits – Hobo Spider Relatively large cm body and up to 5cm including legs Usually tan to brown No true identifying marks for us non-entymologists Fast – run up to 1m/sec Bites and venom usually only cause local damage, but few case reports of systemic toxicity exist

Culprits – Hobo Spider Tegenaria agrestis
Leading cause of necrotic arachnidism in western states/provinces

Bite of the Brown Recluse (and Hobo)
Causes both local and systemic toxicity by means of endothelial cell damage, lysis of red blood cells, coagulopathy, and complex activations such as calcium-dependent systems Sphingomyelinase D is unique to Loxosceles venom and appears to be the major dermonecrotic factor SMD causes platelet aggregation & thrombosis, leading to ischemic and inflammatory tissue damage

Bite of the Brown Recluse
Almost painless bite at first Within few hours pain increases and gets erythematous In more severe cases may see necrotic blebs develop Are “Red, White, Blue” areas of Erythema, Vasoconstriction, Necrosis Progresses to ulcers that may not maximize for 2 weeks Then eschar formation that take months to heal

Photo Courtesy of Dr. M. Francis

Bite of the Brown Recluse – Local Tx
Local wound care and tetanus Analgesics as indicated No proven treatments for necrotism Dapsone touted, but little evidence and can lead to methemoglobinemia and hemolysis on its own Treatments tried: Steroids, hyperbaric oxygen, cyproheptadine None with convincing results Ulcer may progress for weeks! Corrective surgery, such as skin grafting or debridement with closure, should be delayed for 4 to 8 weeks

Bite of the Brown Recluse – Systemic
Systemic Toxicity is quite rare Thought to occur in children or with arterial delivery of venom. Systemic symptoms onset in hrs Leads to: Nausea/Vomiting/Arthralgias and Myalgias Severe evenomations lead to hemolysis, coagulopathy and DIC Coagulopathy and DIC are leading causes of death

Serial hemoglobin, hematocrit, platelet, urinalysis Obtained based on clinical picture: type and crossmatch (perform early), LFTs and coagulation studies Analgesic/antipyretic agents Systemic corticosteroids for hemolysis Methylprednisolone, 10–40 mg IV q6h for 3–5 days Disseminated intravascular coagulation—specific management Packed red blood cell transfusions as needed for anemia Other blood products/components as indicated Dialysis as needed for renal failure Symptomatic and supportive care No commercially available antivenom

Spider Review Black Widow Brown Recluse Hobo
Red Hourglass on underside Venom causes release of neurotransmitters Symptoms are cramps/pain Treat symptomatically/supportively There is an antivenom. Use if life threatening tachycardia and hypertension unresponsive to usual ICU care Brown Recluse Has violin on back and 3 pairs of eyes Bite can lead to necrotic skin lesions Supportive care with prn skin grafting in 4-8 wks Can have systemic toxicity with hemolysis and DIC Steroids and supportive care for this Hobo If see necrotic arachnidism in Canada, it is likely the hobo Treat like the Brown Recluse bite, but less likely to see systemic symptoms

Flashback 27 yr old male presents with a snake bite to his lower leg (out in the badlands of Alberta) His Vitals: HR 90, RR12, BP120/80 afebrile, Sat 99%

Flashback There is slowly spreading area of inflammation and edema on his leg He has nausea and perioral tingling His coag profile is normal. What grade of evenomation is this? Outline how you would treat this patient.

Fin Dowload has Hot/Cold injuries

Cold Injuries

Cold Injuries Local Systemic / Hypothermia

Local Cold Injuries Frostnip Frostbite (most common)
Cold injury without tissue loss Frostbite (most common) Cold injury with tissue loss Chilblain / pernio Cold injury due to chronic dry cold Immersion / Trench Foot Cold injury due to cycles of near freezing in wet environment

Physiology See marked vasospasm Skin pallor
15oC See marked vasospasm Skin pallor Episodes of cold induced vasodilation (Hunting Reflex)

Physiology - Prefreeze
<10oC Vasospasm and endothelial dysfunction Causes plasma leakage to extracellular space Intracellular fluid shifts to extracellular space and intracellular dehydration particularly in endothelial cells

Physiology - Freeze Ice crystal formation intra & extracellularly
<0oC Ice crystal formation intra & extracellularly Disruption of cellular function, especially the endothelial cells leading to large amounts of edema Stasis and microthrombosis – leads to ischemic tissue damage and inflammatory responses

Presentation  Painful  White/blanching with times of erythema
 Loss of sensation Appears white / mottled Loss of fine motor control Loss of gross motor control Tissues appear rigid and waxy  Frozen tissue

Degrees of Frostbite Seen after rewarming 1st Degree 2nd Degree
Erythema, paresthesias 2nd Degree Clear fluid filled blisters, erythema 3rd Degree Deep frostbite, develops hemorrhagic blistering 4th Degree Involves muscles, tendon, bone

Treatment Immersion in 40-42oC water
Treat until tissues become pliable and capillary refill returns Will require analgesia as rewarming hurts Local wound care Update Td Most severe frostbite is admitted and given BID-TID whirlpool sessions and ROM therapy No surgical amputation for 8-12 wks minimum (until shows extent of tissue loss) Frostbite in January, amputate in June

I’m OK, right doc?

Oh, it must be Summer now…

Long Term Tx Autoamputation in severe cases Neuropathic Pain Syndromes
Autonomic Dysfunction Anatomical restriction of movement

Hypothermia

Physiology of Heat Loss

Definitions Hypothermia <35oC Mild 32-35oC Moderate 28-32oC
Characterized by mild changes and shivering thermogenesis Moderate 28-32oC Loss of shivering presence of atrial arrythmias Severe <28oC Ventricular arrythmias

Pathophysiology CNS CVS Renal Mild Resp/GI

Hypothermic Brain 34oC Amnesia&Dysarthria 33oC Ataxia 32oC Stupor
29oC Marked LOC 27oC Loss of reflexes and voluntary motor 25oC CNS blood flow 1/3 of norm due to loss of autoregulation 23oC No corneal or oculocephalic reflexes 19oC Flat EEG

Hypothermic Heart >32oC May see tachycardic or bradycardic response
<32oC Bradycardia due to prolonged depolarization phase of pacemaker cells <32oC Atrial arrythmias <32oC Osbourne J-Waves <28oC Ventricular arrythmias <24oC Significant hypotension <18oC Asystole

Osbourne J-Waves

Cold Kidneys Peripheral vasoconstriction initially leads to an increased effective circulatory volume This leads to diuresis (cold diuresis) May lead to naturesis (not in all) Then see progressive decreased GFR as temperature drops (GFR is 50% normal at 30oC) Leads to fluid/salt abnormalities

Resp and GI Be aware of cold bronchorrhea due to decreased ciliary function Decreased GI motility as core temperature drops

Investigating Hypothermia
Use rectal temperature probe – best correlates with core temperature Need low temperature thermometer Most of our TM probes, etc only go to 35oC If you see a low temp, think of checking with a low temperature thermometer

EKG May see prolongation of almost any EKG intervals Cardiac arrythmias Osbourne J-Waves

ABGs Often see metabolic acidosis due to lack of perfusion and oxygenation Much debate in literature about warming/not warming ABGs on analyzer. It doesn’t really matter CBC Increased Hct due to cold diuresis 2% in Hct for every 1oC drop in temp Electrolytes Most common abnormality is hypokalemia Due to shift of K+ into muscles not a kaliuresis Most often corrects with rewarming

Hypothermia and ACLS ACLS care is different
Hypothermic patient has markedly abnormal circulation Has impaired receptor functions Decreased liver metabolism

Hypothermia and ACLS Airway management as usual Breathing as usual
Shown to be safe and does not induce arrythmias Paralytics may not work in severe hypothermia Breathing as usual Be aware of cold bronchorrhea Circulation If an arrest rhythm and temp <30oC then consider defib at 200J x1 only (some guides say up to x3) CPR ‘You’re not dead until warm and dead’ No drugs recommended until temp >30-32oC Fluid trial of cc NS/D5W

Rewarming Strategies Active Passive Active External Rewarming (AER)
Active Core Rewarming (ACR) Invasive (lavage, CPB) Simple (Warmed IV/O2)

Passive Rewarming Remove wet clothing Cover in blankets, etc
Allow patient to rewarm on own (i.e. shivering) Appropriate for mild hypothermia as patient has intact shivering thermogenesis Often not enough for moderate to severe hypothermia

Active External Rewarming
Provide external heat source Warmed blankets, radiant heat sources, ‘Bair Hugger’ Appropriate for mild and moderate hypothermia Get core temp rises of about oC/hr

Active Core Rewarming-Simple
Warmed, humidified O2 Warmed IV fluids (Level I blood warmer for fluids) Appropriate for mild/mod/severe hypothermia Get temp rises of 0.5-2oC/hr with each

Active Core Rewarming-Invasive
Warmed Bladder Irrigation Gastric Lavage Peritoneal Irrigation Closed Thorasic Lavage Each modality will raise temp ~ 1oC/hr Cardiopulmonary Bypass Can raise temp by 1-2oC / 5 min Hemodialysis

Active Core Rewarming-Invasive
Ann Emerg Med 16:1042, 1987 ACR - Active core rewarming AER - Active external rewarming ET - Endotracheal tube GBC - Gastric-bladder-colon lavage IV - Intravenous NT - nasotracheal tube P - peritoneal lavage PER - passive external rewarming

Indications for Extra Corporeal Rewarming (Bypass)
Severe hypothermia Cardiovascular instability Failure to rewarm by conventional techniques Completely frozen extremity Rhabdomyloysis with severe hyperkalemia

Approach Temp Passive AER ACR-Simple ACR- Invasive 32-35 C Yes Yes/No
Usually no <28 Or <32 and unstable

Core Temperature Afterdrop
Theory is that as you warm the patient’s extremities the vascular beds open up and cold blood returns to the circulation Consider truncal rewarming in mod to severe hypothermia True clinical relevance is uncertain Note on study of self cooling/rewarming in bath w temp probes in self

Summary Local cold injuries Hypothermia
Frostnip, frostbite, immersion, Chilblain Rewarming and local care Delayed amputation Hypothermia mild, moderate, severe Effects: CNS, CVS, Kidney Rewarming Passive Active External Active Core Rewarming

10 minute break!

Flashback You’re in the south on a camping trip after your ‘little three day quiz’ and you find that this critter has nibbled you when you venture to the outhouse.

Flashback The Doc at the local ED scratches his head and says ‘I dunno…’ What do you advise him about your expected course and treatment?

Heat Illness

Heat Loss We are biochemical furnaces
Without heat management mechanisms we would see body temp rise of >1oC/hr

Heat Management

The Heating-Cooling System

Heat Illnesses Minor Illnesses Major Illnesses Miliaria (Heat Rash)
Heat Edema Heat Syncope Heat Cramps Major Illnesses Heat Exhaustion Water Depletion Salt Depletion Heat Stroke Classical Exertional

Miliaria/Heat Rash/Prickly Heat
Plugging of eccrine sweat glands Occurs under clothing area Itchy at first then get inflammatory eruptions Sometimes secondary staph infection Treat with cooling, cleaning May last 1-2 weeks

Heat Cramps Occur with work in hot environments
Copious sweating during exertion Usually fluid replacement with insufficient sodium Often after exertion get cramps (i.e. after work, not during activity) Treat oral Na/water replacement or IV NS

Major Heat Illness Mild Severe Heat Exhaustion Heat Stroke

Heat Exhaustion Volume depletion under conditions of heat stress
Presents with malaise, fatigue, headache Temp usually <40oC NEURO FUNCTION is NORMAL If unsure if this is heat exhaustion or heat stroke, treat it as heat stroke Classically described as either salt or water deficiency. Usually a combo of both

Heat Exhaustion – Water & Salt
Water Deficit Occurs with inadequate fluid replacement when working in hot environment See progressive hypovolemia Treat with cooling and fluid replacement Salt Deficit Takes longer to develop and occurs with sweat loss and hypotonic fluid (water) replacement Characterized by hyponatremia, hypochloridemia Treat with cooling and hyponatremia therapy

Heat Stroke Exogenous hyperthermia Loss of thermoregulatory function
Signs of severe CNS dysfunction Coma, seizures, other neuro defects Temp usually >40oC Often see dry hot skin (but not always)

Classic vs. Exertional Heat Stroke
Age Elderly Younger Health Impaired Good Activity Sedentary Strenuous Drug Use Diuretics, anticholinergics, antipsychotics, antihypertensives Usually none Sweating No Profuse Lactic Acidosis Usually no, but poor prognosis if present. Yes, is not prognostic Rhabdo Unusual Often Hyperuricemia Modest Severe Acute Renal Failure <5% ~30% Hypocalcemia Uncommon Common DIC Mild Marked CK Mild Elevation Severe Elevation Hypoglycemia Cause Poor Heat Dissipation Excess Heat Production

Treatment ABCs as usual Rapid Cooling Judicious Fluids
Consider hyperK+/rhabdo in exertional heat stroke contraindicating succinylcholine Rapid Cooling Cool Water Immersion Evaporative Cooling (wet skin and fans) Adjuncts: ice packs, lavage, etc. Judicious Fluids Most only require modest IV fluids (i.e. 500cc NS)

Cooling Ice Water Immersion Likely faster cooling
Challenges to patient management if: Decreased LOC Seizure Evaporative Cooling Spray with tepid water and use fans May be slower cooling Better patient access for treatment

Cooling

Cooling Aim for a temperature of 39oC
Then stop active cooling (don’t want hypothermia) If severe shivering (such that cannot cool) consider chlorpromazine 25mg IV

Heat Stroke’s Complications
It doesn’t take long to fry and egg or a brain Hypotension is common and tricky as can be from multiple causes Dehydration responds to fluids Hypodynamic heart (increased CVP, PCWP, low CO) may require pressors Hyperdynamic heart (increased CVP, PCWP,CO) require modest fluid and very aggressive cooling So consider CVP/SwannGanz monitoring in hypotensive heat stroke patient not responding to judicious fluids

May get pulmonary edema of lungs Centrilobar necrosis of the liver almost always evident by 24-72hr post with large increases of LFTs Renal Failure Due to poor perfusion and rhabdo

Coagulopathies Poor prognostic sign See with purpura, bleeding (CNS, lung, GI) Manage with cooling and supportive care

Review Minor: Miliaria, Heat Cramps Major: Heat Exhaustion and Stroke
IF ANY DOUBT TREAT AS HEAT STROKE Cooling to 39oC Supportive care

Environmental Emergencies

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