Archive for the ‘EM2’ Category


In EM2 on July 11, 2011 at 1:36 pm
46 yo M c/o L sided CP, intermittent x 3 weeks. Pain is worse with exertion or bending fwd. Associated with shortness of breath  (SOB). Better with some positions.
Vitals: BP-117/82     HR-93      RR-20        92% on RA. 100% on 3L
Labs were all unremarkable and troponin was negative .

CXR on presentation

Old CXR one month prior

How does the new CXR compare to the old?
What bedside maneuver/study can you (the EM resident) perform to make the diagnosis?
What is the difference between a pericardial effusion and pericardial tamponade?
What are the indications for pericardiocentesis in the ED?
What is the technique for performing pericardiocentesis?
Differential diagnosis for a new or worsening pericardiac effusion?
Teaching Points to follow…

How does the new CXR compare to the old?
This is an obvious point BUT Always ‘look at’ and try to read your own images; compare new to old images, call radiology early if something looks suspicious or unclear.
The new CXR was read as: Enlarged cardiac silhouette may represent cardiomegaly and/or pericardial effusion, with small bilateral pleural effusions.
What bedside maneuver/study can you (the EM resident) perform to make the diagnosis?
a bedside ULTRASOUND (US)! never underestimate the usefulness of this tool that is now available in many urban EDs. In a patient presenting with chest pain, shortness of breath and an enlarged cardiac silouhette on CXR, its important to quickly figure out if that silouhette is secondary to an effusion that is ‘potentially’ causing a tamponade and as a result, the patient’s symptoms.
The EM resident in this case did do a bedside Ultrasound: The pericardial sac, myocardium, and 4 chambers were identified. Large circumferential pericardial effusion with some degree of ra and rv diastolic collapse. Enlarged interatrial septum.
Read here for more on the usefulness of bedside US.  

What is the difference between a pericardial effusion and pericardial tamponade?
Think of is this way – an effusion is a noun while tamponade is a verb!
 Normally, the pericardial space contains only about 15-60cc of ultrafiltrate plasma which serves as a lubricant between the visceral and parietal components of the pericardium.
Pericardial effusion is an abnormal accumulation of fluid within the pericardial sac around the heart. Its usually slowly accumulating and patients with effusions are usually asymptomatic. it takes about 200-250cc of pericardial fluid to show up on CXR as cardiomegaly. Effusions can be transudative (due ‘fluid overload’, CHF, hypoproteinemia) or exudative (due malignancy or infection) depending on the etiology.
Cardiac tamponade is the physiologic phenomena that depends most importantly on the rate of fluid accumulation. Tamponade occurs when the pressure in the pericardium is sufficient to overcome and inhibit right ventricular filling, decrease cardiac compliance and thus decrease cardiac output. This happens when fluid accumulates fast within the pericardial sac – faster than the rate of parietal pericardium stretching and faster than the body’s ability to increase blood volume and support RV pressures. The Classic triad we are always taught for Cardiac tamponade is hypotension, muffled heart sounds, and distended neck veins.
EKG typically shows decrease voltage or more rarely, electrical alternans.

Notice every other R wave alternates amplitude. This is due to the change in the size of the R vector being conducted as the heart floats in a large effusion and move away and towards the chest wall (i.e the EKG lead).

Differential diagnosis for a new or worsening pericardiac effusion?
Cancer! Uremia from renal failure, Post infarct myocardial rupture, aortic dissection, iatrogenic cardiac perforation. In trauma, always think penetrating chest injury!
What are the indications for pericardiocentesis in the ED? 
The indication for emergent pericardiocentesis is the presence of life-threatening hemodynamic changes in a patient with suspected cardiac tamponade

What is the technique for performing pericardiocentesis?
Simply performing the classical ‘blind’ subxiphiod approach aiming towards the patient’s left shoulder has HIGH Morbidity and complications (unintentional liver biopsies, gastric perforations, myocardium injury etc) and is really unnecessary with the ever so useful bedside ultrasound!
Check out this website for technique on ultrasound guided pericardiocentesis HERE
Outcome: Cardiology was called to bedside after the bedside ultrasound was performed. US guided pericardiocentesis was performed – 1L of hemorraghic fluid drained. Pericardial window was placed the next day.

this is the patients CXR after the pericardiac drain was placed. If you look closely, you can find the drain on this XR.


Chapter Review: Brain and Cranial Nerve disorders

In EM2 on May 5, 2011 at 8:20 pm

Cerebral Venous Thrombosis

It’s a rare entity but should be on our radar. Just like the peripheral venous system, the cerebral venous system may be predisposed to and form thrombus that cause major problems for the patient.

Risk Factors: head and neck infections (sinusitis, otitis media, facial cellulitis etc), trauma, surgery, tumor, pregnancy, dehydration, hypercoagulable states(protein C or S disease, antithrombin III deficiency, factor V leiden etc)), oral contraceptive use.
Clinical Features: headache (primary feature, in 74-90%), papiledema, seizures, altered mental status, lethargy. Cranial nerve palsies may also be present.

Diagnostic strategies: the ‘gold standard’ is cerebral angiography, however, the test of choice is an MRI with MRV. CT scan is not sensitive or specific enough to confirm or exclude the diagnosis but it may rule out other diagnosis on the differential and it may show the presence of an infarct that doesn’t follow an arterial distribution as a hint.

Treatment: Initial management is similar to that of a patient with acute stroke: ABC’s! keep the head of bed elevated or patient in reverse trandelenberg to prevent increase in ICP. IV heparin has been shown to be beneficial. Catheter-based intervention with thrombolysis (i.e tPA) may be helpful but for now is mostly reserved for patients that are rapidly deteriorating neurologically, with  an elevated ICP, or with decreased level of consciousness. Surgery (i.e local thrombectomy) may be indicated in patients with significant deficits who are unresponsive to intense medical treatment.

Disposition: Admit – stroke unit or ICU depending of severity/stability of patient.

Multiple Sclerosis

An inflammatory demylinating neurological disease with a genetic predisposition. Affects multiple parts of the CNS with deficits manifesting in cognitive, cranial nerve, motor, sensory, bowel/bladder and sexual functions.CN II is the most commonly affected cranial nerve, manifesting as optic neuritis (usually the first symptom)

Management: acute MS exacerbation is often handled with IV methylprednisone (250-500mg bid for 3-7days). Treatment of complications include baclofen (for spasticity), propranalol or benzo’s (for tremors or ataxia).

RUSH – Rapid Ultrasound in SHock.

In EM2 on April 20, 2011 at 1:00 am

Here’s a pretty amazing article/protocol that serves as a guide to help the EP(emergency physician) in integrating resuscitative ultrasound early in the care of the undifferentiated hypotensive medical patient.

I suggest everyone reads this article. It provides a great review of shock, explains the concepts in some details and reviews ultrasound techniques . Here’s the general gist…

Classifications of Shock.

1. Hypovolemic shock – e.g in trauma with massive hemorrhage, internal blood loss (GI Bleed, AAA rupture) or loss of body fluids (vomiting, diarrhea)

2. Cardiogenic shock – e.g cardiomyopathy, myocardial infarction, acute valvular failure.

3. Distributive shock – e.g sepsis, anaphylaxis, neurogenic shock

4. Obstructive shock – e.g cardiac tamponade, large pulmonary embolism, tension pneumothorax.

RUSH exam – the shock ultrasound protocol

3steps: 1. the pump, 2. the tank, 3. the pipes. 

1. The pump – this refers to the heart i.e the patients cardiac status. A bedside echo can be use to evaluate the pericardium, cardiac contractility, and heart strain.

4views: parasternal long, short, apical 4view and subxiphoid view.

Contractility – the ‘squeeze’ of the heart. A normal healthy heart should have a large amount of change between diastole to systole i.e. a vigorously squeezing heart should almost obliterate the ventricular cavity during systole. Therefore with ultrasound(US), a poorly contracting heart can be easily visualized as moving little between the cardiac cycle. The EP can tell if the contractility is good, intermediate or poor. The focus is not necessarily to identify wall motion abnormality. Also knowing the strength of left ventricular (LV) contractility can help give a better idea of how much fluid the heart can tolerate before signs of overload become apparent. An enlarged LV that’s significantly dilated can lead to diagnosis of left heart failure/systolic failure.

The pericardium – an apparent pericardial effusion with signs of right ventricular(RV) collapse indicate a tamponade physiology. Ultrasound should also be used in performing emergent pericardiocentesis at the point of maximum fluid collection.

Heart strain – An enlarged RA (right atrium) or RV relative to the LV indicates that there’s a strain in the pulmonary system, likely a massive central pulmonary embolus, leading to acute dilation of the right ventricle. In the scenario of a hypotensive patient, thrombolysis may be considered.

2. The tank – this involves evaluation of the IVC and IJ to assess how ‘full’ they are in terms of size and collapse with inspiration.

View: epigastric long axis view of the IVC.

In normal physiology, the IVC collapses with inspiration secondary to increasing intra-thoracic pressure. This respiratory variation can be augmented with forceful inspiration i.e. ‘the sniff test’. A small caliber (<2cm) IVC with more than 50% collapse on inspiration correlates roughly with a CVP of <10cm H2O – this may indicate a hypovolemic/distributive shock state. A larger caliber (>2cm) IVC with less than 50% collapse on inspiration roughly correlates with a CVP of >10cmH2O – this may indicate more of a cardiogenic/obstructive shock state.

**this physiology is skewed in patients who are intubated or in patients who received vasodilators or diuretics prior.

Ultrasound can also evaluate tank leakiness (with a FAST exam looking for intra-abdominal fluid), tank compromise (as in a pneumothorax) or tank overload (as in pulmonary edema)

3. The pipes – US views of major arteries and veins can identify immediately like threatening i.e. in pipe Rupture as in a massive AAA (abdominal aortic aneurysm) or a aortic dissection. Venous obstruction can also be evaluated with compression sonography of deep veins of the lower extremities (DVT)

Find the full article:

The RUSH Exam: Rapid Ultrasound in SHock in the Evaluation of the Critically lll Emergency Medicine Clinics of North America – Volume 28, Issue 1 (February 2010) 29-56

Abdominal pain

In EM2 on February 16, 2011 at 4:38 am

55yo M hx HTN presenting with one day of abdominal pain. diffuse, non-specific. states he’s felt constipated x1day. denies nausea or vomitting. tried to force a BM today, noted BRBPR. was seen in pmd office today, sent to ED for concern of abdominal bruit. no prior hx of AAA or abdominal surgeries.

PE: vital signs stable: BP 146/93, HR 106, RR 11, 93% on RA. Pt visibly uncomfortable, +Tenderness on deep palpation of lower abdomen bilaterally. heart/lungs otherwise within normal. +BRPPR(bright red blood per rectum). Bedside Ultrasound – AAA @9cm. ?rupture.

Outcome: STAT Vascular surgery consult. labs, CTabdomen/pelvis CT read: Infrarenal abdominal aortic aneurysm measuring up to 10.8 cm with stranding within the left adjacent anterior and posterior pararenal space concerning for rupture. hgb/hct 14.5/42.4; Creatinine = 0.4;  Patient went straight to the OR.  Patient remained awake and interactive throughout ED course (albeit emotional and tearful upon notification of his diagnosis).

Teaching point: diagnosis and acute management of AAA.

1.Clinical Suspicion (let your alarm bells ring!): Risk factors are males, hypertension, smoker, Artherosclerotic vascular disease, first degree relative with AAA, age>65. Regardless, it is imperative to maintain a high clinical suspicion for AAA even in the setting of normal vital signs. In patients >5oyo with acute abdominal/back/flank pain, the idea of a AAA should cross the EM physicians mind at least as part of the differential. Classic triad of pain, hypotension and abdominal mass is only present about 30% of the time. AAA rupture has about 80% mortality and any patient with large AAA should be considered unstable 2/2 potential to rapidly de-compensate.

Patients presenting with GI bleed complaints (melena or hematochezia) may have an aorto-enteric fisutla (may be primary – with an initial AAA or secondary after AAA repair). GI bleed is initially minor in the first few days but may progress to massive hemorrhage.

Patients presenting with high-output cardiac failure may have an aorto-venous fistula. This is when the AAA erodes into the IVC thus causing a shunt of blood into the IVC.

Patient may presenting with subacute back/flank pain that started sharp initially, subsided but is still persistent. There’s a concern of a low-grade retroperitoneal leak from the AAA. CT may show a chronic/organized hematoma which may be confirmed in the OR.

2. Imaging: BEDSIDE ULTRASOUND(US) is your friend! its quick, non-invasive and has a sensitivity/specificity approaching 100% for ruling in a AAA; shortens time to diagnosis and time to OR, can be done at bedside (great for the unstable patient that cant be transported to radiology). It may be limited by body habitus and excessive bowel gas. After age 50, the normal diameter of the infrarenal aorta is 1.5 cm in women and 1.7 cm in men. Aorta>3cm is considered AAA. an US can rule in/out a AAA. its harder to state if its ruptured based on US; A FAST exam can be done to evaluate for free fluid. AAA: <4cm – annual close monitoring with US; 4-5cm – q6mths US. >5cm – elective repair (20-40% risk of rupture).

CT scan: about 100% accuracy. will give better information about rupture, retroperitoneal bleed, or dissection.

3. Surgery consult: this should be done ASAP! before labs and before CT(if diagnosis is made on US). Patient is only ‘stable’ once they are in the OR with their aorta cross clamped!

4. Medical management: this is temporal until the patient can get definitive treatment in the OR. You know the drill: IV, O2, monitor, 2large bore IV’s. If patient is hypotensive, begin initial fluid resuscitation BUT what they really need is BLOOD. Get on the phone with blood bank, get that O(-) blood and start transfusing. Airway control as needed depending on patients’ mental status.

Post op complication: Graft infection, Aorto-enteric fistula, Pseudoaneurysm, Endoleak.

Refrences: Rosen’s 6th edition, chpt 85.

Stroke Syndromes

In EM2 on February 6, 2011 at 4:05 am

Just a post to remind us of common stroke syndromes.

Remember the homonculus and the circle of willis?

The stroke syndromes are divided by anatomy. Just look at the circle of willis to find the artery, then look at the homunculus to correlate the expected deficit. Remember, right handed people are Left hemisphere dominant and 80% of left handed people are also left hemisphere dominant. Thus only about 20% of people are right hemisphere dominant. If stroke occurs in a non-dominant hemisphere, it will usually manifest as neglect, inattention, agnosia.

Anterior circulation – motor and sensory deficits.

1. Anterior cerebral artery (ACA) stroke –  Motor deficits: contralateral leg, foot, arm paralysis. Sensory deficit: lower>>upper extremities. Loss of frontal lobe control – personality change, gait apraxia, incontinence.

2. Middle cerebral artery(MCA) stroke – most common site of intracranial thrombosis. Motor deficit: contralateral hemiplegia upper extremity weakness > lower extremity; Sensory deficit: contralateral hemianesthesia, aphasia.

3. Posterior cerebral artery (PCA) stroke – PCA supplies the occipital cortex thus a stroke will manifest as loss of vision, cortical blindness, contralateral homonymous hemianopsia, change in mental status, visual agnosia. Ipsilateral cranial nerve 3 palsy

Posterior circulation – ipsilateral cranial nerve deficits + contralateral motor deficits

4. Vertebrobasilar artery stroke – difficult to detect. ipsilateral cranial nerve deficits and cerebellar signs: vertigo, ataxia,nausea/vomitting, vertical/bilateral nystagmus, dysmetria(abnormal finger-nose test), dysdiakokinesis (asking patient to rapidly turn over the fingers and tap the palm with the back of them, repeatedly).

  • Wallenberg Syndrome – Proximal vertebral artery infarct. Lateral medullary syndrome.

5. Basilar artery stroke – ‘locked in syndrome’ – loss of all motor functions asides from upward gaze, +coma.

6. Lacuna Infarct – occlusion of small, perforating arteries of the deep subcortical areas of the brain, cause by small vessel disease from HTN and DM. Presents as pure motor, pure sensory, and ataxic hemiparetic strokes


In EM2 on February 6, 2011 at 2:29 am

55yo M s/p recent L craniotomy/Neck Sg in 1/11 for metastatic lung ca to brain presenting with persistent Hiccupps x3days. no resolving, constant. denies any neurological complaints. no focal weakness or numbness.
+Hiccups on exam, neuro exam negative, otherwise well appearing male. CTHead – unchanged, no acute findings, + post-op changes. CXR – redemonstration of LLLobe mass, unchanged.

Outcome: pt given IV torazine 25mg with resolution of symptoms. Hiccups returned, given IV valium 2.5mg with resolution of symptoms. dc’ed home with chlorpromazine rx, f/u with neurosg and PMD.

Teaching point: Treatment of persistent hiccups.

A hiccup is an involuntary, intermittent, spasmodic contraction of the diaphragm and intercostal muscles. A hiccup ’bout’  consists of episodes lasting <48hrs. Persistent hiccups last >48hrs. Intractable hiccups last >1mth.

Differential Dx for persistent/intractable hiccups is extensive. In the patient above, most likey ddx will be vagal nerve irritation from recent surgery or tumor irritating the recurrent laryngeal n.

Treatment – First line is Chlorpromazine – only med thats FDA approved to treat hiccups, (**also the board answer** 🙂 ). IV  better than PO. Dose is 25mg PO TID x7-10days. Remember it may cause dystonic reaction and drowsiness.

Other meds: Metoclopramide, Valium.

High blood pressure

In EM2 on February 3, 2011 at 5:54 am

45yo M presenting for evaluation for high blood pressure. Patient denies any complaints (head or chest pain, shortness of breath, abdominal pain, nausea or vomiting). BP 173/85 on arrival. Chronic hypertensive, non-compliant with medication x1mth, just got his new prescription filled but hasn’t taken any medication.

Outcome: Patient was counseled on negative outcomes of poorly controlled HTN including stroke, renal failure, heart attacks and aortic dissection.

42yo M presenting with severe diffuse HA x 1day, BP 205/100, denies CP,SOB or other complaints. Pt has a history of hypertension, non-compliant with medications. Labs were unremarkable. CTHead negative.

Outcome: Pt was given IV labetalol 10mg – BP reduced to 160/90. Headache was treated symptomatically. Patient improved and was discharged home.

Teaching Point: Management of high blood pressure.

As a frequent complaint in the ED, its important for the EM physician to know when to ‘jump into action’ and when to just offer carefully crafted counseling to will the most unlikely patient into compliance. 😀

Definition: Malignant HTN = diastolic BP>110mmHg + signs of end organ damage.

Malignant HTN and Hypertensive crisis are almost interchangeable. Goal BP control = 25% reduction in MAP(mean arterial pressure) in the first hour and then more slowly after that.

What are your options in terms of medication? You want something titratable i.e an IV medication.

BBlocker – Labetalol (dose 20mg bolus, then 1-2mg/min titrated up), Esmolol (ultra-short acting, typically used to combat reflex tachycardia caused by vasodilators. dose 500µg/kg over 1min, gtt @ 50-100µg/kg/min)

Vasodilator – Nitroprusside (drug of choice in most cases. prolonged use increases risk of cyanide toxicity (an active metabolite. dose 0.25-1µ/kg/min), Nitroglycerin, Hydralazine(traditionally used in pre-eclampsia/eclampsia, may also cause reflex tachy);

AceI – Enalapril;

alpha-blocker – Phentolamine

NOTE in Intracranial Hemorrhage(ICH) – HTN is usually a consequence of ICH but can be as a result. officially, anti-hypertensive medications is NOT indicated and may be harmful in acute stroke syndromes. However clinically, BP control is often initiated to maintain a MAP between 90-110. Remember, too tight a controlled BP in this case may worsen outcome by promoting ischemic damage.

Emergency Drug of Choice
Hypertensive encephalopathy Nitropusside
ICH (intracranial hemorrahge) Labetalol
Cardiac Ischemia Nitroglycerin, Betablocker
Acute pulmonary edema Nitroglycerin
Aortic dissection Nitropusside + BetaBlocker
Preclampsia/Eclampsia Labetalol
Adrenergic Crisis Phentolamine





In EM2 on January 15, 2011 at 5:19 pm


3 month old Male presenting with parents to the ED for cough x2days, congestion and one epeisode of vomitting. Parents denies fever, chills, sick contacts or other symptoms. Baby otherwise looks well, tolerating po and making wet diapers. immunizations UTD. Full term delivery, no complications at birth, on no medications otherwise. PE unremarkable, well appearing baby, Sa02 98% on room air. Labs: RSV+

Outcome: discussed with patient’s pediatrician, scheduled follow up in 2days, otherwise patient was dc’ed home with close instructions to parents to return if symptoms worsen or patient has trouble breathing.

4week old M brought into the ED with cough x3days, congestion and L eye crusting. [+]sick contacts but otherwise no complications at birth, full term, no medical hx or medications. PE shows mild bilateral conjunctival injection and oral thrush but otherwise good air exchange, SaO2 98% on room air, well appearing baby. Labs: RSV+

Outcome: transfered to children’s hospital for admission.

Teaching Point: When to admit for RSV infection

Overiew: RSV is a very common cause of upper respiratory track infection in infants and children during winter and spring months.  typically manifests as bronchiolitis or pneumonia. Spread via hand-hand contact, or contact with respiratory droplets (3-8dy incubation period). Typically presents clinically with cough, wheezing, decrease po intake.

Factors associated with more severe disease, thus supporting admission are:

age<3months at time of infection, prematurity (<35wks) at birth, children of multiple births(>3), oxygen saturation <95%, Toxic appearance on exam, RR>70 on room air, congenital lung or heart disease, neuromuscular disease, atelectasis or pneumonitis on CXR.

Management: If the baby is well appearing, well hydrated and tolerating PO intake without any of the factors listed above, management is typically symptomatic with close follow up in a few days with the patient’s pediatrician. Bronchodilators have not been shown to be particularly beneficial.

If the baby doesnot look well or have any of the factors above, then they should be hospitalized, and care is typically supportive as well (supplemental oxygen, IVF, bronchodilators). Aerosolized Ribavirin can be used in severe cases however its expensive and has not been shown to particularly reduce hospitalization or mortality. Typically, children hospitalized for RSV infection, do well and are discharged in a few days. They do have a higher incidence of subsequent wheezing in the future.



Rosen’s 6th edition, chapter 128 pg 2051.

eMedicine: RSV (see link here)


Chapter Review: Hypothermia

In EM2 on January 9, 2011 at 11:12 pm

Physiology of Heat loss.

Core Body Temp is between 36.5-37.5C. Heat is lost via 4 main mechanism radiation, evaporation, conduction and convection. At cold temperatures (32-37C), the body attempts to generate heat primarily via shivering, but also with  vasoconstriction, increased catecholamine, thyroid and adrenal output. At T<32C, there’s loss of the shivering mechanism. At T<28C, loss of endocrine regulation and metabolic rate slows down by 50%.

Hypothermia: core Temp < 35C (95F)

Etiology: increased loss of heat (accidental heat loss, burns, iatrogenic), impaired thermogenesis(CNS impairment, trauma, ETOH)  or impaired thermoregulation(endocrine etiologies eg. thyroid). In the ED typically seen in age extremes, homeless people without adequate shelter, alchoholics.


****get CORE temp with rectal, bladder or esophageal probe(low-reading temperature probe). NOT oral  or tympanic temp. Careful to ensure that you are not taking the temp of really cold stool 🙂 technically, the gold standard for getting the temp is with a pulmonary artery catheter – but this has obvious limitations.***

Mild Hypothermia (T: 32-35C) – tachypnea, tachycardia, shivering, ‘cold diuresis’, dysarthria

Moderate Hypothermia (T: 28-32C) – altered mental status, CNS depression, paradoxical undressing, hyporeflexia, Afib, bradycardia, slow respiratory rate

Severe Hypothermia(T<28C) –  hypotension, bradycardia, asystole/VF, coma, areflexia.

EKG: prolonged PR, QRS and QT intervals. + Osborn(J)waves. Classic progression is: bradycardia –>Afib –> slow ventricular rate –>V.Fib –>asystole

Workup :

no trends in electrolytes (watch for K 2/2 rhabdomyolysis or acidosis), hyperglycemia (insulin is inactive at T<30C)

H/H – hemoconcentrated – 2/2 diuresis, volume contraction and increase in HCT(by 2%) with every 1c drop in temp; leukopenia and thrombocytopenia may occure 2/2 splenic sequesteration.

Coags – hypothermia causes a prothrombotic state/DIC -picture likely 2/2 inactivation of coagulation cascade enzymes. Lab work may be falsely normal cause labs typically warm blood samples to 37C before running them.

CXR may show aspiration pneumonia, pulmonary edema.

Management – goal is T>32 at 0.5-2C/hour (or as fast as possible)

Think: is this patient mildly or profoundly hypothermic? what is their risk for cardiac dysrhythmia?

ABCDE – airway(intubate as indicated, provide warm humidified air either via ETT or Face mask), Breathing, Circulation (will likely require tons of warm(40-42C) IVF; low dose pressors may be indicated if refractory to fluid resuscitation but typically donot work until patient is rewarmed), Disability (GCS/intubate), Exposure(remove wet clothing, reduce agitation, keep patient warm and dry)

CPR: chest compressions should be held off if the patient has a frozen chest OR has any HR. With patient with a HR, chest compressions may agitate myocardium and lead to Vfib. Take 45-60sec palpating for a pulse before determining there is none and initiating CPR. Femoral access is the best option for central line access because there’s no risk of irritating the myocardium with the guidewire and the site is easily compressible.

Treatment of arrythmia: Defibrillation for VF and ACLS medication should be attempted ONCE but is pretty futile if core temp is <30C. Active rewarming should commence immediately if its unsuccessful. Atropine is typically not useful for bradycardia(since its not vagally mediated); Lidocaine is not typically useful for arrythmia. Bretylium has not been strongly proven to help.


Passive External Rewarming – for mild hypothermia (therefore requires that the patient still has a physiologic response to cold to assit with rewarming measures). Remove wet clothes, Keep patient dry and warm with blankets. [results in core temp increase of 0.5-4c/hour]

Active external rewarming – bair hugger, warm IVF(you can heat up NSS to 40-42C – 1L bag for 2mins on high settings), hot water bottles at axilla, groin, extremities. [The bair hugger and similar gadgets typically cause about 1.5c/hr temperature increase]. Watch out for ‘Core temp afterdrop’ – occurs when trunk and extremities are rewarmed simultaneously, causing acidic cold blood in the extremities to return to the core and drop temp. Rewarming Shock – occurs when cold patient is removed from cold environment, causing peripheral vasodilation and shunting of blood from the core, resulting in hypotension.

Active Internal Rewarming : generally indicated in patients with hemodynamic compromise and/or ventricular arrythmias. Peritoneal dialysis with dialysate temp at 40-42C, heat irrigation(via thoracic lavage, NGT and [Foley with warm fluids – limited heat transfer 2/2 limited surface area]), Extracorporeal Blood rewarming (hemodialysis, cardiopulm bypass, Continuous arteriovenous rewarming, venovenous rewarming) – performed in cardiac arrest, when other measures have failed; warms at 2-4C/hr. CPB can rewarm up to 9.5c/hr!

Failure to rewarm(<0.6C/hr)? check and correct hypoglycemia(glu), AI (IV hydrocortisone), hypothyroid (IV levothyroxine), start empiric antibiotics (patient with hypothermia and sepsis have worse outcomes).

Further reading: the Jan 2011 Critical Decision Journal (from ACEP) has a great hypothermia write up – its emailed to EM residents for free. Check it out!

Chapter Review: Frost Bite

In EM2 on January 5, 2011 at 3:53 pm

Overview: Frost Bite is a dry cold related injury caused by freezing tissue. Typically seen in military/combat situations, homeless people, outdoor activity/athletics or in people with blunted self-protective instincts.

Pathophysiology: Cold temperature causes vasoconstriction and shunting of blood away from periphery towards the core to reduce heat loss. Tissue freezes at ZERO(0) degrees C. Frost bite injury occurs in 2phases:

  1. Ice crystal formation extracellularly causing extracellular fluid shift resulting in cell death once 1/3 of volume is lost.
  2. Stasis, sludging and cessation of blood flow. This could lead to microvascular collapse.

Clinical Presentation: 75% present with numbness. Patients also complain of clumsiness, heaviness/’clunk of wood’ sensation in extremities, pain, throbbing and electric-shock sensation in the affected part.

good prognosis: clear bullae, healthy appearing skin, positive sensation to pinprick

Poor Prognosis: ‘frostbite’ looking skin, hemorrahagic bullae, cyanosis.

4 degrees of injury:

  1. Erythema and anaesthsia
  2. Clear blisters, edema
  3. Hemorrhagic blisters, eschar formation in weeks
  4. full thickness injury involving muscles, bones and tendons


General principles: keep affected area dry. remove all wet clothing. avoid vigorous rubbing. avoid partial rewarming: it’s better to transport a frozen part rather than initiate and then incomplete rewarming techniques.

ED management:

  1. Initiate rapid thawing by immersion of affected part in water at 40-42C (thermometer measured).  if >42C, may result in subsequent thermal injury.
  2. Provide parenteral analgesia during rethawing, it can be painful! Morphine or Toradol
  3. Rewarming typically takes 20-40mins and is complete when affected part ‘flushes'(erythema)
  4. Debride clear vesicles/blisters, LEAVE hemorrhagic blisters alone (since they represent damage to sub-dermal vasculature).
  5. Update Tetanus
  6. Consider IV PCN for strep prophylaxis in severe cases
  7. Check Labs- typically not helpful unless there’s underlying hypothermia, dehydration or sepsis from wound infection. Baseline Xrays should be obtained however Radiology is typically used if there’s suspected underlying fractures or dislocations.
  8. After rewarming, keep area dry and elevated.
  9. If Cyanosis persist after re-warming techniques, consider compartment syndrome (which may not be appreciated due to cold-induced loss of pain sensation)  as a diagnosis and measure compartment pressures.

Disposition: Most patients (except in mild cases) are admitted for 24-48hours. Surgical consult for long term management is warranted. Inpatient immersion hydrotherapy(baths) 30mins TID is typically indicated.

Frost bite injuries DONOT automatically warrant surgical management i.e. amputation. It takes up to 1-3months for viable tissue to heal and non-viable tissue to ‘declare’ itself. Think “Frostbite in January, amputate in July”. Recently due to advancement in radiologic evaluation of tissue, surgical decisions about grafts and amputations can be made in about 1 month. The amount of tissue eventually salvaged often exceeds even initial optimistic estimates

Sequelae are numerous including paresthesias, ‘electric-shock’ sensation, dermatologic changes, arthritis, muscular atrophy and many more.