FOAMcastini – SMACC Day 3

(ITUNES OR Listen Here)

We are bringing you pearls from conferences we attend including SMACC (#smaccUS).  This conference was amazing and we enjoyed meeting everyone.  We look forward to seeing y’all at SMACC in Dublin June 13-16, 2016 and hope you check out the Free Open Access Medical education (FOAM) lectures from SMACC, in podcast form, until then.

Things in medicine aren’t always engineered to help us succeed. Engineering the environment smarter may make care safer. – Kevin Fong

  • Medication vials often look quite similar and in a busy, heated moment this may lead to medication errors.  Check out the EZdrugID project.
EZdrugID
Photo: Dr. Nicholas Chrimes

Analgesia, there’s more to it than medicine – Jeremy Faust

  • Distraction is a good thing.  Doing a painful procedure such as injecting local anesthetic? Distract the patient in tactile fashion by lightly scratching the patient proximal to the procedure. Alternative, music and videos can distract children and adults.
  • Calm music may reduce perception of pain.
  • Take advantage of child life, if you have them [AHRQ]!

The Glasgow Coma Scale is a problem – Mark Wilson (see this blog post)

  • The score doesn’t have intrinsic meaning. A GCS score can be associated with mortality ranging from 20-57%, depending on the individual components [Healey]
  • We’re really bad at assigning correct GCS scores to patients, even when we have cheat sheets [Feldman]
  • The interrater reliability of the GCS is abysmal [Bledsoe, Gill]
  • Describe the patient’s exam!

Shift work is disruptive – Haney Mallemat

  • Microsleep is dangerous, yet fairly common in the over tired provider
  • Replacing traditional night shifts with “casino shifts” may help.  These are often comprised of 2 short shifts from 10p-4a and 4a-10a with the notion that each provider would get sleep during the “anchor period” of the Circadian cycle, 2am-6am.  Small studies have shown this feasible, preferred by many, and perhaps perceived [Croskerry, Dukelow]
PlayPlay

Episode 30 – Thyroid

(ITUNES OR Listen Here)

The Free Open Access Medical Education (FOAM)

This week we cover Dr. Scott Weingart’s EMCrit episode on Thyroid Storm

Diagnosis: Hyperthyroid, Fever, Altered Mental Status, Sympathetic Surge, Precipitating Event

Treatment (PPID – PTU, propranolol, iodine, dexamethasone or MIEH – methimazole, iodine, esmolol, hydrocortisone):

  • Supportive care – IV fluids, identify trigger (infection, DKA, trauma, etc)
  • Block production of thyroid hormone: Methimazole or Propothiouracil (PTU)
  • Block thyroid hormone release: Iodine (wait 60 min after giving methimazole or PTU)
  • Calm the sympathetic surge: beta-blockade (propranolol – also inhibits conversion of T4 to the more active T3, metoprolol or esmolol)
  • Block conversion of T4 to T3 and prevent adrenal insufficiency: steroids (dexamethasone, hydrocortisone)
From Rosh Review

Core Content
Rosen’s Emergency Medicine (8e) Chapter 128, Tintinalli (7e) Chapter 223

Thyroid disorders exist on a spectrum from myxedema coma to thyroid storm, with a large area in between.

Hyperthyroidism – too much thyroid hormones only from the thyroid gland

Thyrotoxicosis –  too much thyroid hormone from any cause (i.e. taking too much thyroid supplement)

Thyroid Storm – see above. Thyrotoxicosis with  increased adrenergic hyperactivity or abnormal response to the thyroid hormones by the peripheral tissues

Myxedema coma – These patients are the opposite of thyroid storm, all the systems are depressed (they are essentially hypo-everything).  The diagnosis is clinical but these patients will have significantly elevated TSH with low T3/T4.

  • Altered mental status
  • Hypothermic, <35.5°C (95.9°F)
  • Hypotensive
  • Bradycardic
  • Hyponatremic
  • Hypoglycemic

Treatment

  • Intravenous levothyroxine (T4) although endocrine may recommend that some patients get intravenous T3
  • Supportive care – passive rewarming, dextrose, intravenous fluids
  • Steroids
  • Identify underlying cause

Generously Donated Rosh Review Questions 

1. A 28-year-old woman with no past medical history presents to the emergency department with acute dyspnea. Physical exam reveals tachycardia, warm extremities, wide-pulse pressure, bounding pulses, a systolic flow murmur, exophthalmos and a neck mass. [polldaddy poll=8935230]

2. [polldaddy poll=8936552]

Answers

1. This patient most likely has high-output heart failure secondary to thyrotoxicosis. High output heart failure occurs when cardiac output is elevated in patients with reduced systemic vascular resistance. Examples include thyrotoxicosis, anemia, pregnancy, beriberi and Paget’s disease. Patients with high output heart failure usually have normal pump function, but it is not adequate to meet the high metabolic demands. In high output heart failure the heart rate is typically elevated, the pulse is usually bounding and the pulse pressure wide. Pistol-shot sounds may be auscultated over the femoral arteries, which is referred to as Traube’s sign. Subungual capillary pulsations, often referred to as Quincke’s pulse, may be also be present. Although these findings may be seen in other cardiac conditions, such as aortic regurgitation or patent ductus arteriosus, in the absence of those conditions, these signs are highly suggestive of elevated left ventricular stroke volume due to a hyperdynamic state. Patients with chronic high output also may develop signs and symptoms classically associated with the more common low-output heart failure; specifically, they may develop pulmonary or systemic venous congestion or both, while maintaining the above normal cardiac output.

Low output heart failure (C) is often secondary to ischemic heart disease, hypertension, dilated cardiomyopathy, valvular and pericardial disease or arrhythmia. It can cause dyspnea but is not associated with symptoms of a hyperdyanmic state. Aortic regurgitation (A) is classically associated with bounding pulses, a wide pulse pressure and subungual capillary pulsations; however, aortic regurgitation is less likely in a young woman with no past cardiac history. Additionally, this woman has exophthalmos and a goiter on exam, which support the diagnosis of thyrotoxicosis. Methamphetamine intoxication (D) usually presents with agitation, tachycardia, and psychosis; however, it is not associated with a hyperdynamic state, exophthalmos or a goiter.

2.  Hyperthyroidism is a condition in which there is overproduction and increased circulation of thyroid hormone. Hyperthyroidism has a variety of causes and variable presentation. Increased circulating thyroid hormone causes a hypermetabolic state and increases beta-adrenergic activity. Initially, patients may have vague constitutional symptoms. As the disease progresses, clinical manifestations may become more organ-specific. Thyrotoxicosis or thyroid storm represents the most severe manifestation of the disease. Thyroid storm is life threatening and characterized by hyperadrenergic activity. Patients present with vital sign abnormalities including tachypnea, tachycardia, hyperthermia and hypertension. ECG may show atrial dysrhythmias like atrial flutter and fibrillation or simple sinus tachycardia. High-output cardiac failure is common as well. Physical features include goiter, opthalmopathy and tremors. Patients will also have increased reflexes and altered mental status. Thyroid storm treatment involves suppression of thyroid hormone synthesis and secretion, prevention of peripheral conversion from T4 to T3 and blocking the peripheral adrenergic stimulation. Blocking the peripheral effects of thyroid hormone is best accomplished with a beta-blocker and propranolol is preferred as it also decreases conversion of T4 to T3.

Lithium (A) is a cause of hypothyroidism. In hyperthyroidism, TSH is depressed (C). Weight gain (D) is common in hypothyroidism.

Theme Music:  Flippen performed by The Punch Brothers, used with permission

PlayPlay

Episode 29 – Hyperglycemia

(ITUNES OR Listen Here)

The Free Open Access Medical Education (FOAM)

We review a post on Pediatric DKA from Dr. Anton Helman’s Emergency Medicine Cases.

 Pearls from this episode:

  • Fluids come first in DKA but you may not need as much as you think. They recommend only using fluid boluses, and even then a baby bolus of 5-10 cc/kg, in the hypotensive decompensated patients, coupled with frequent re-assessments.  Other patients can get up to twice maintenance of 0.9% NaCl.
  • No insulin bolus for pediatric patients, ever.
  • Cerebral edema is the most dreaded complication of DKA and seems to be associated with severe presentations, young children (<5), or DKA as the presentation of diabetes.  Treatment related factors such as administration of an insulin bolus or sodium bicarbonate may also contribute. The role of fluids (particularly over-aggressive fluids) is less clear [1-3].
  • Management of cerebral edema: ABCs, Elevate head of the bed 30 degrees, Mannitol 0.5-1g/kg IV over 20min AND/OR hypertonic (3%) NaCl 5-10cc/kg IV over 30min

The Bread and Butter

We cover hyperglycemia including diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). We do this based on  osen’s Emergency Medicine, Chapter 126 (8th ed) and Tintinalli, Chapter 222 (7th ed). But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

 Diabetic Ketoacidosis

Diagnosis – glucose >250 mg/dL, pH <7.3, bicarbonate <18, anion gap >10

Workup – evaluate electrolytes (particularly potassium) and potential triggers for DKA.

Treatment – fluid resuscitation is initial intervention as these patients are typically 4-6 L down.  In adults we hold insulin treatment until we know the patient’s serum potassium, as these patient’s are depleted secondary to osmotic diuresis.  Further, the patient’s serum potassium may be falsely elevated by acidosis.  Insulin may be started once the potassium is >3.5 (with potassium replacement if <5.3).  We do not bolus pediatric patients but the ADA guidelines and Rosenalli state we do not need the insulin bolus in adults either [4-6].  The use of subcutaneous insulin in DKA is popular amongst pediatric patients and growing in popularity in adults [7,8].

Screen Shot 2015-06-02 at 11.19.08 AM

Hyperosmolar Hyperglycemic State (HHS)

Diagnosis – elevated serum glucose (often >600 mg/dL), serum osmolar >315-320 mOsm/kg. Patient’s may have a concomitant acidosis or ketosis, but this is often less profound than in DKA.

Workup – ascertain why the patient ended up in HHS – whether it was a mobility issue or polypharmacy (diuretic, lithium, etc). Check osmolality and for DKA.

Treatment – these patients are often severely dehydrated (>8 Liters). Start with volume resuscitation and add an insulin infusion (0.1 units/kg/hr).

 

Generously Donated Rosh Review Questions 

1. A 43-year-old man presents with altered mental status. His vital signs are HR 113, BP 143/63, T 98.9°F and blood glucose of 750 mg/dl. During your evaluation he has a brief generalized tonic-clonic seizure. [polldaddy poll=8904849]

Answers

1. This patient presents with signs and symptoms consistent with hyperglycemic hyperosmolar state (HHS) and intravenous fluids should be given aggressively early in management. HHS is a syndrome characterized by dehydration, hyperglycemia, hyperosmolarity and altered mental status. Patients may present with confusion, lethargy, seizures, focal neurologic deficits or frank coma. Pathophysiologically, decreased insulin (or insulin action) leads to gluconeogenesis and increased circulating glucose levels. This in turn draws fluid from the intracellular space into the intravascular space. The resultant osmotic diuresis leads to profound intravascular dehydration, electrolyte abnormalities and hyperosmolarity. Typically, patients will have a blood glucose >600 mg/dl and an osmolarity >350 mOsm/L. Blood urea nitrogen and creatinine are usually elevated. Initial management focuses on supportive care and aggressive fluid resuscitation. Patients with HHS are estimated to be 5-10 liters behind. In addition to fluid administration, electrolyte repletion is paramount.

2. A 45-year-old man presents with altered mental status. On arrival, his finger stick is 35 mg/dL. He is given dextrose leading to the return of a normal mental status. On history, he reports he may have accidentally taken extra medication. Which of the following medications requires prolonged observation in the hospital?

  • Glipizide
  • Metformin
  • Novolog
  • Sitagliptin

In most adults, symptomatic hypoglycemia occurs when glucose levels reach 40 to 50 mg/dL. Glipizide is a sulfonyurea oral hypoglycemic drug. This class of medication is associated with hypoglycemic episodes through their action as an insulin secretagogue. In a sulfonylurea overdose, patients should be observed for 24 hours. When the etiology is unclear, laboratory testing including renal function is indicated. In situations without large ingestions, patients may be discharged if no additional episodes of hypoglycemia occur after an observation period. In cases of severe, prolonged or recurrent episodes of hypoglycemia from sulfonylureas, additional therapy with octreotide as an inhibitor of insulin release is indicated.

References:

  1. Glaser NS, Wootton-Gorges SL, Buonocore MH, et al. Subclinical cerebral edema in children with diabetic ketoacidosis randomized to 2 different rehydration protocols. Pediatrics. 2013;131(1):e73–80. doi:10.1542/peds.2012-1049.
  2. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344(4):264–9. doi:10.1056/NEJM200101253440404.
  3. Lawrence SE, Cummings E a, Gaboury I, Daneman D. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 2005;146(5):688–92. doi:10.1016/j.jpeds.2004.12.041.
  4. Diabetic Emergencies : New Strategies For An Old Disease.
  5. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335–43. doi:10.2337/dc09-9032.
  6. Goyal N, Miller JB, Sankey SS, Mossallam U. Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. 2010;38(4):422–7. doi:10.1016/j.jemermed.2007.11.033.
  7. Umpierrez GE, Cuervo R, Karabell A, Latif K, Freire AX, Kitabchi AE. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care. 2004;27(8):1873–8. Available at: http://www.ncbi.nlm.nih.gov/pubmed/15277410. Accessed July 17, 2014.
  8. Umpierrez GE, Latif K, Stoever J, et al. Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis. Am J Med. 2004;117(5):291–6. doi:10.1016/j.amjmed.2004.05.010.
PlayPlay

Episode 26 – The Spinal Cord

(ITUNES OR Listen Here)

The Free Open Access Medical Education (FOAM)

In January 2015, ACEP recommended against the use of long backboards by EMS, “Backboards should not be used as a therapeutic intervention or as a precautionary measure either inside or outside the hospital or for inter-facility transfers.”

We review the use of longboards and cervical collars for spinal immobilization using posts by Thomas D of ScanCrit (Curse of the Cervical Collar, Cervical Collar RIP,  Cervical Collars Slashed From Guidelines), a post by Dr. Minh Le Cong from PHARM, and this Medest118 post.

The bottom line:

  • The benefits of devices to aid in spinal immobilization such as cervical collars and long backboards are controversial.  Guidelines and protocols are continuing to recommend judicious use of these devices.  Examples include:
    • Clearing collars in obtunded blunt trauma patients with negative high quality CT [EAST]
    • Selective application of cervical collars [ILCOR]
    • No backboards and selective pre-hospital immobilizaiton [ACEP]

The Bread and Butter

We differentiate between spinal shock and neurogenic shock, cover the incomplete cord syndromes (anterior cord, central cord, Brown-Sequard Syndrome), and fly through some of the cover using Tintinalli (7e) Chapter 255; Rosen’s (8e) Chapter 43, 106  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Spinal shock – Reduced reflexes following think of this as a stunning of the spinal cord.

Neurogenic shock –  This is loss of sympathetic innervation from injury to the cervical or thoracic spine, typically from a cervical or upper thoracic spinal cord injury, resulting in bradycardia and hypotension.

  • Warm, peripherally vasodilated , and hypotensive  from loss of sympathetic arterial tone with a relative bradycardia from unopposed parasympathetic (vagal) tone
  • Typically presents within 30 minutes, can last 6 weeks
  • Diagnose only after excluding other sources of shock
  • Treatment: crystalloid, vasopressors

Incomplete Cord Syndromes

 Better prognosis than complete cord syndromes. Means there is some sensory or motor preserved distal to lesion (i.e. rectal tone or perineal sensation)

Anterior Cord Syndrome 

  • Complete loss of motor, pain, and temperature below but retain posterior columns (position and vibration)
  • Flexion injury or decreased perfusion (aortic surgery or injury)
  • Paralysis and hypalgesia below the level of injury with preservation of posterior column (position and vibration)

Central Cord Syndrome

  • Sensory and motor deficit, often associated with hyperextension injuries (think whiplash)
  • Affects arms>legs
  • Think MUDE (pronounced muddy): Motor, Upper, Distal, Extension (injury)

Brown-Sequard Syndrome

  • Classically associated with a stab wound
  • Loss of motor function and position and vibration on ipsilateral side with contralateral loss of pain and temperature (fibers cross)

 Reflex Review

C4 Spontaneous breathing: “3-4-5 keep the diaphragm alive”
C5 Shoulder shrug
C6 Flexion at elbow:  think flexing your elbow up to drink before…
C7 Extension at elbow: …extending it to set a drink down.
C8-T1 Flexion of fingers
T1-T12 Intercostal and abdominal muscles
L1-L2 Flexion at hip
L3 Adduction at hip
L4 Abduction at hip
L5 Dorsiflexion of foot
S1-S2 Plantar flexion of foot
S2-S4 Rectal sphincter tone: “2-3-4 keeps your junk off the floor”

Generously Donated Rosh Review Questions 

Question 1. A patient arrives to the ED 15 minutes after being involved in a MVC. He is conscious, and there is no obvious trauma. He is immobilized on a long spine board with a cervical collar in place. His BP is 60/40 mm Hg and HR is 60 bpm. His skin is warm.

[polldaddy poll=8775757]

Question 2. [polldaddy poll=8776250]

Answers

1.  A. Loss of deep tendon reflexes is expected. Neurogenic shock occurs after an injury to the spinal cord. Sympathetic outflow is disrupted resulting in unopposed vagal tone. The major clinical signs are hypotension and bradycardia. Patients are generally hypotensive with warm, dry skin because the loss of sympathetic tone impairs the ability to redirect blood flow from the periphery to the core circulation. The most commonly affected area is the cervical region, followed by the thoracolumbar junction, the thoracic region, and the lumbar region. The anatomic level of the injury to the spinal cord impacts the likelihood and severity of neurogenic shock. Injuries above the T1 level have the capability of disrupting the spinal cord tracts that control the entire sympathetic system leading to the loss of deep tendon reflexes.Neurogenic shock must be differentiated from “spinal” shock, which refers to neuropraxia (B) associated with incomplete spinal cord injuries. This state is transient (C) and resolves in 1 to 3 weeks. Alpha-1 vasopressors (e.g., phenylephrine), in addition to dopamine, norepinephrine, and epinephrine (D), should be used to maintain blood pressure and ensure organ perfusion.

2. C.  In the anterior spinal cord syndrome, just the posterior columns are preserved and so patients lose all pain and temperature sensation as well as motor function. Most cases of anterior cord syndrome follow aortic surgery, but it has also been reported in the setting of hypotension, infection, vasospasm, or anterior spinal artery ischemia or infarct. In trauma, typically hyperflexion of the cervical spine causes the injury to the spinal cord.

Loss of all motor and sensory function (B) occurs with a complete transection of the spinal cord. Most commonly this occurs after a significant trauma. Isolated motor function loss (A) is not a classic syndrome and would result from a small area of injury on the cord just involving the corticospinal tract. Upper greater than lower motor weakness occurs (D) with a central cord syndrome. Sensory involvement is variable although burning dysesthesias in the upper extremities may occur. Most commonly the syndrome occurs after a fall or motor vehicle accident.

PlayPlay

FOAMcastini – Kappa

(ITUNES OR LISTEN HERE)

Reading papers is hugely important but learning how to read medical literature is an entirely different realm and many of us have statsphobia.

The Free Open Access Medical Education (FOAM)

Kappa – It’s Greek To Me

The Bread and Butter

Kappa – a coefficient indicating the degree of inter-rater reliability.  How reliability are people getting the same result for a certain test or evaluation?

  • For example, you would want two people looking at the same chest x-ray to agree on the presence or absence of an infiltrate. Sometimes, chance comes into play and kappa tries to account for this.  Similarly, clinical decision aids are often comprised of various historical and physical features.  It would be nice if different clinicians evaluating the same patient would turn up the same results (thereby yielding the decision aid consistent and reliable).

To see how to calculate kappa, check this out.

The value of kappa ranges from -1 (perfect disagreement that is not due to chance) to +1 (perfect agreement that IS due to chance).  A value of 0 means than any agreement is entirely due to chance [1-2].

kappa

People debate over what a “good” kappa is.  Some say 0.6,  some say 0.5 [1-2]. In the PECARN decision aid, for example, the authors only included variables with a kappa of 0.5 [3-4].

Limitations:

  • Prevalence – if prevalence is high, chance agreement is also high.  Kappa takes into account the prevalence index; however, raters may also be predisposed to not diagnose a rare condition, so that the prevalence index provides only an indirect indication of true prevalence, altered by rater behavior [6].
  • The raters – agreement may vary based on rater skill, experience, or education.  For example, when PECARN variables were looked at between nurses and physicians, the overall kappa for “low risk” by PECARN was 0.32, below the acceptable threshold as this number suggests much of the agreement may be due to chance [6].
  • Kappa is based on the assumption that ratings are independent (ie a rater does not know the category assigned by a prior rater).

References
1. Viera AJ, Garrett JM. Understanding interobserver agreement: the kappa statistic. Fam Med. 2005;37:(5)360-3.

2. McGinn T, Wyer PC, Newman TB, et al. Tips for teachers of evidence-based medicine: 3. Understanding and calculating kappa. CMAJ. 2004;171 (11)

3.Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374:(9696)1160-70. [pubmed]

4. Gorelick MH, Atabaki SM, Hoyle J, et al. Interobserver agreement in assessment of clinical variables in children with blunt head trauma. Acad Emerg Med. 2008;15:(9)812-8.

5. Nigrovic LE, Schonfeld D, Dayan PS, Fitz BM, Mitchell SR, Kuppermann N. Nurse and Physician Agreement in the Assessment of Minor Blunt Head Trauma. Pediatrics. 2013.

6. de Vet HC, Mokkink LB, Terwee CB, Hoekstra OS, Knol DL.  Clinicians are right not to like Cohen’s κ 2013;346:f2125

PlayPlay

Episode 24 – Mild Traumatic Brain Injury/Concussion

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

We cover the Taming the SRU podcast, “Ketamine Cagematch” (iTunes), a debate between Dr. Minh Le Cong and Dr. Chris Zammit.

Dogma persists that ketamine may increase intracranial pressure, which would be bad in traumatic brain injury (TBI) given the fixed space in the cranial vault.  These are largely from Yet, these patients often need sedation, for agitation or intubation, and drops in blood pressure are also deleterious (see EMCrit on neuroprotective intubation).

PRO (Le Cong): The literature doesn’t show clinically significant deleterious outcomes from ketamine use in the head injured patient.  Review in Annals on ketamine and ICP.  Deleterious effects of apnea may result from other sedative agents.

CON (Zammit): Studies showing that ketamine does not increase ICP confounded by the presence of other sedatives on board.  As a result, there may still be a risk to using ketamine in these patients.

The Bread and Butter

We cover key points on concussion and mild TBI from Tintinalli 254 but to be honest, Rosenalli is lacking on this topic so we’ve turned to the ACEP clinical policy, AAN guidelines, Ontario Pediatric Guidelines, and the  AAP guidelines on the topic.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Mild TBI and concussion are often referred to interchangeably and the definition varies [1-3].  Unfortunately, concussion is often thought of only in the sports population and not all-comers to the Emergency Department (ED) so patients may not receive proper .

Definition: Essentially, any alteration in mental status following head injury. Per the CDC:  Head injury from blunt trauma or acceleration/deceleration with GCS 14-15 PLUS

  • observed or self-reported transient confusion, disorientation, or impaired consciousness
  • Amnesia around the time of injury
  • Signs of other neurologic or neuropsychological dysfunction
  • Any loss of consciousness (LOC) less than 30 minutes (!) [3]

For more on how reliable LOC is in these patients, see this post.

Causes: Falls and motor vehicle collisions are the most common causes in adults, whereas sports are the more common in kids.

  • The effects on the brain are largely a result of “secondary injury,” consistent of alterations in ion-channel, metabolic pathways, and electrochemical imbalances.  These are more functional than structural.

Symptoms: There’s a good bit of overlap with migraine, more significant head trauma, and symptoms that may be confused for behavioral issues in younger populations.

Screen Shot 2015-02-19 at 1.27.09 PM

Testing: Not all head injuries require imaging.  Certainly, patients with focal neurologic findings warrant imaging; yet, in other cases, validated decision aids exist to help determine which patients may or may not need imaging.  In adults, we like the Canadian CT Head tool , although the ACEP clinical policy uses the New Orleans Criteria.  For a solid review of the two, check out this SGEM episode.  In children, consider the use of the PECARN decision aid. Otherwise, a good neurologic exam and observation should suffice.

Something to consider – patients often believe that a “normal” CT scan of the head means that they don’t have a concussion.  As a result, they may not take concussion precautions seriously.  In this case, imaging may provide false reassurance.

There’s increased attention on biomarkers like GFAP, total tau, and S-100B but these are not ready for prime time and are not incredibly specific [3].  Further, standardized assessment tools such as SCAT3 and ACE may be useful, but are used predominantly on-site for sports related incidents.

Treatment

  • Education – this is one of the biggest areas in which ED providers may make a difference. Give patients or family members precautions for concussion, even if the injury or mechanism seems relatively mild.  Studies show that a majority of pediatric patients do not follow up as instructed after a concussion [4].  Perhaps communication of the the potential gravity of concussion and long-term implications may improve follow up.
  • Rest – This the is the mainstay of initial treatment for most mild TBI [1-3, 5].  It’s unclear how strict this rest needs to be, but a recent study in the pediatric literature found no benefit to strict rest versus standard instructions (1-2 days rest + graduated return) [6].
  • Graduated return to activity – after a period of rest, it’s recommended to slowly resume activities, spending at least 24 hours at each level of increased activity.  If an individual gets symptomatic, they should return to the level of activity at which they were asymptomatic (see the Zurich protocol).
  • Return to play – clearing people from the ED is NOT a good idea.  For those on the sidelines, a player should be removed from activity for the day after a suspected concussion.

Why do we care in the ED?

  • Quality of Life – Concussive symptoms can be quite disabling.  Giving patients a name for their symptoms, resources, and education may help them understand the process of recovery and available resources.
  • Second Impact Syndrome – A second head injury in a patient symptomatic from a concussion may experience diffuse cerebral edema, possibly from loss of cerebral autoregulation.* [2]
  • Post Concussion Syndrome (PCS) – a subset of the concussion population will have persistence of symptoms which, if they persist > 1 week to 3 months after the injury, is deemed PCS. *  This is thought to be more prevalent in individuals with a history of depression, anxiety, or migraines and in those with more severe ED presentations [2].
  • Bouncebacks – Patients may present to the ED with symptoms of concussion but may not give a history of significant trauma.  Remember that concussion may occur after a seemingly minor bump to the head and elderly may need extra support with activities of daily living or may bounce back with a more life threatening injury.
  • Lack of follow up.  While some may follow up with concussion specialists, the majority of our patient population lacks the ability for meaningful or specialist follow up.  We can’t assume that someone else is going to guide our patients through concussion recovery or that when we write “follow  up with _____” that it will happen.  Our care may be it, make it good.

*The literature on these is sparse and complicated by variable definitions, information, and standardized reporting.

 Generously Donated Rosh Review Questions (scroll for answers)

Question 1. A 33-year-old man with no past medical history presents with a headache 3 days after a closed head injury. The patient states that he stood up from kneeling and hit the top of his head on a wood cabinet. There was no loss of consciousness or seizure activity. In addition to the headache, he complains of difficulty concentrating at work and dizziness. His physical examination is unremarkable.[polldaddy poll=8663736]

Question 2. A 42-year-old man is brought to the ED after he tripped and fell while he and his wife were on a walk. His wife notes that she saw him hit his head on the pavement and that he did not respond to her for 45 seconds. When he started to respond, she says that he was very confused. In the ED, his vital signs are BP 135/75, HR 88, RR 14, and oxygen saturation 98% on room air. On exam, you note some minor lacerations on the patient’s upper extremities, face, and scalp and his GCS is 15. As the wife recounts what happened, the patient does not recall any of the events and continuously asks to repeat what happened to him. A CT scan of the brain is normal. The patient is diagnosed with a concussion and is ready to be discharged from the ED. [polldaddy poll=8663741]

References

1. Tavender EJ, Bosch M, Green S, et al. Quality and consistency of guidelines for the management of mild traumatic brain injury in the emergency department. Acad Emerg Med. 2011;18:(8)880-9. [pubmed]

2. Haydel M.  Management Of Mild Traumatic Brain Injury In The Emergency Department. Emergency Medicine Practice.  September 2012 Volume 14, Number 9

3. Jagoda AS, Bazarian JJ, Bruns JJ, et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med. 2008;52:(6)714-48. [pubmed]

4.Hwang V, Trickey AW, Lormel C, et al. Are pediatric concussion patients compliant with discharge instructions? J Trauma Acute Care Surg. 2014;77(1):117–22; discussion 122.

5. Brown NJ, Mannix RC, O’Brien MJ, Gostine D, Collins MW, Meehan WP. Effect of cognitive activity level on duration of post-concussion symptoms. Pediatrics. 2014;133(2):e299–304.

6.Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135:(2)213-23. [pubmed]

Answers

 1.  D.  The patient presents with minor head trauma and complaints consistent with a concussion and should have neurology follow up arranged. A concussion is a minor TBI that is often seen in MVCs and collision sports (football, hockey). It is typically caused by a rotational injury or an acceleration-deceleration injury. Patients will present with a number of non-specific symptoms including headaches, dizziness, confusion, amnesia, difficulty concentrating, and blurry vision but do not have focal neurologic findings. Despite the absence of severe intracranial injury, patients can have chronic and debilitating symptoms from concussions. Neurology referral is recommended, as patients should have functional testing and tracking of their symptoms for resolution. It is vital to counsel patients to avoid contact sports or activities that increased the risk of recurrent injury as these patients are at risk for more severe injury with second impact.In the absence of focal neurologic findings, absence of antiplatelet or anticoagulant use and minor trauma, imaging is not needed (A, B, C).

2. Cerebral concussions are clinically characterized by headaches, confusion, dizziness, and amnesia for the event. Concussions are characterized by a transient loss of consciousness that occurs immediately following blunt, nonprenetrating head trauma, caused by impairment of the reticular activating system. Concussions present without focal neurologic deficits, and CT and MRI show no acute abnormalities. Although not commonly performed for concussions, functional imaging, such a PET scan, may show changes in blood flow and glucose uptake. It is critical to inform the patient and his or her family of the second impact syndrome (SIS), which occurs when a patient suffers a second concussion after being symptom-free from the first. Although SIS is more common in sports based injuries, especially among teenagers, the risk of serious sequelae following a second concussion is immense. Due to neurochemical and autoregulatory changes that may still be present, a second concussion soon after a first generally produces a rapid neurologic decline that proves fatal. Patients should be told to avoid activities that could cause falls or trauma for at least 1 week after the patient is completely asymptomatic from the first concussion. Most patients with a concussion can be discharged from the emergency department and advised to follow-up with a primary care physician within 1 week (B). Although some patients have only transient symptoms from a concussion, others may experience persistent symptoms termed postconcussive syndrome (PCS).  PCS symptoms most often include headache as well as memory, sensory, sleep, and concentration disturbances. It is important to consider PCS in all patients with a concussion, but a primary care physician is generally able to care for these patients. It is unnecessary to obtain an MRI (C).  Although patients should avoid trauma and falls for at least 1 week after being completely asymptomatic after the first concussion, a change insleeping position (D) is unnecessary.

PlayPlay

FOAMcastini – Reflections on ACEP tPA Clinical Policy Update Draft

(iTunes or Listen Here)

As detailed in this FOAMcastini, ACEP just released a draft of an updated clinical policy on tPA for acute ischemic stroke.  This came in the wake of years of controversy over the aggressive position taken in the 2012 clinical policy.

While FOAMcast is not an interview style podcast, we felt compelled to get some perspective on Emergency Physicians a little more experienced than ourselves.  Here we interview:

Dr. Ryan Radecki (@emlitofnote), Assistant Professor, University of Texas – Houston

  • We don’t know who best benefits from tPA so elucidating which patients are “carefully selected” may get hard.
  • See his response to the policy on his blog here

Dr. David Newman (#draftnewman), Associate Professor of Emergency Medicine, Mount Sinai Hospital

  • The process for ACEP clinical policy creation seems to work.  The constituency expressed concern and the college listened and went back and re-created the policy from the bottom up.
  • This policy reflects a move from content expert to methodologists which better reflects the evidence compared with opinions (and is the standard per USPSTF).

Dr. Anand Swaminathan (@EMSwami), Assistant Professor of Emergency Medicine, NYU

  • Inclusion of more rigorous methodology and review of evidence.
  • May be perceived as too “soft” by tPA supporters.  This policy may not overtly change practice but may open up avenue of conversations.

Dr. Ken Milne (@thesgem), Chief of Staff at South Huron Hospital

  • When looking at “carefully selected” patients, as noted in the policy, remember to use the Evidence Based Medicine trifecta of evidence, patient values, and clinical expertise.  In isolation, one component is not sufficient.
  • Previous discussions of NINDS, and the Cochrane tPA article
PlayPlay

Episode 22 – The Knee

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

This week we’re covering a post from the incredible pediatric resource, Don’t Forget the Bubbles, “Knee X-ray Interpretation” by Dr. Tessa Davis.  We use a systematic approach to assessing chest x-rays, so why not knee x-rays?

  •  Know the anatomy
  •  Look at:
    • Effusion
    • Main bones
    • Tibiofemoral alignment
    • Tibial plateaus
    • Intercondylar eminence
    • Patellar tendon disruption
    • Patellar fracture

The Bread and Butter

We summarize some key topics from Rosenalli, that’s Tintinalli (7e) Chapter s271, 281; Rosen’s (8e) Chapters 57, 136.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Knee Dislocation

  • Anterior is most common (40%), posterior (33%)
  • Approximately 50% of knee dislocations may be relocated upon presentation to the hospital (this does not reduce risk of badness)
  • Most worrisome sequelae = popliteal artery disruption.  Of patients with popliteal disruption, the amputation rate rises to 90% 8 hours after the injury without surgical intervention.
  • Workup may depend on your institution (ex: angiogram vs. CT angio vs. ultrasound) but all patients will need an ABI + 24 hour of pulse checks per current standards.
Screen Shot 2015-01-08 at 1.10.48 PM
Algorithm (adopted from Rosen’s)

Septic Arthritis

  • Most Common Organisms: S. aureus, N. gonorrhea
  • Hematogenous spread
  • Most Common Location: knee, hip

Risk factors such as immunocompromised hosts and use of steroids are risk factors for septic arthritis but the ones with the highest likelihood ratio (LR+ >10 is ideal):

  • Skin infection overlying prosthetic joint (LR+ 15)
  • Joint surgery within the preceding 3 months (LR+ 6.9)
  • Age > 80 (LR+ 3.5)

Diagnosis:  In the red, hot, swollen, painful joint, think septic arthritis.  Clinical and laboratory indicators aren’t great. Synovial fluid analysis, particularly the culture exists as the gold standard.  Arthrocentesis Trick of the Trade from ALiEM. Here are the operating characteristics from Margaretten et al:

  • Fever: Sensitivity 57%
  • Lab tests: White Blood Cell count (WBC), sedimentation rate (ESR), and c-reactive protein don’t perform well
    • WBC LR+  1.4 (1.1-1.8); LR- 0.28 (0.07-1.10)
    • Erythrocyte sedimentation rate 1.3 (1.1-1.8); LR- 0.17 (0.20-1.30)
    • C-reactive protein  1.6 (1.1-2.5); LR- 0.44 (0.24-0.82)
  • Synovial fluid gram stain and culture is the “gold standard.”

Treatment: Intravenous antibiotics and washout of the joint by orthopedics in the operating room

 Generously Donated Rosh Review Questions 

Question 1. A 67-year-old man with a history of gout presents with atraumatic left knee pain. Physical examination reveals an effusion with overlying warmth and erythema. There is pain with passive range of motion. He reports a history of gout in this joint in the past. [polldaddy poll=8568492]

Question 2.  A 27-year-old woman presents with severe left knee pain after an MVC where she was the front passenger. She states her knee hit the dashboard. An X-ray of the patient’s knee is shown below. After reduction, the physical examination reveals swelling of the knee and an Ankle-Brachial Index (ABI) of 0.8. [polldaddy poll=8569540]

Screen Shot 2015-01-12 at 5.13.06 PM

Answers.

1. D. Septic arthritis is a bacterial or fungal infection of a joint typically spread hematogenously unless there is direct bacterial contamination. The synovium is highly vascular and lacks a basement membrane making it susceptible to bacterial seeding. Certain conditions predispose individuals to septic arthritis including diabetes, sickle cell disease, immunocompromise, alcoholism or pre-existing joint disease like rheumatoid arthritis or gout. Fever is present in less than half of cases of septic arthritis so with clinical suspicion an arthrocentesis is indicated. The knee is the most common joint affected and patients have pain (especially on passive range of motion) and decreased range of motion often accompanied by warmth, erythema and fever. This patient may have an acute gouty flare, but the clinician must exclude an infection. On joint fluid analysis, the white blood cell count of a septic joint is typically > 50,000. Indomethacin (B) is a non-steroidal anti-inflammatory agent commonly used in the treatment of acute gout. Gout is an arthritis caused by deposition of monosodium urate monohydrate crystals in the joint space. Acute flares involve a monoarticular arthritis with a red, hot, swollen and tender joint. Acute episodes of gout result from overproduction or decreased secretion of uric acid. However, measurement of serum uric acid (C) does not correlate with the presence of absence of an acute flare. A radiograph of the knee (D) may show chronic degenerative changes associated with gout but will not help to differentiate a gouty arthritis versus septic arthritis.

2. C. Obtain Angiography. This patient presents with a knee dislocation and signs of a popliteal artery injury requiring angiography for diagnosis. A knee dislocation refers to a dislocation of the tibia in relation to the femur and not a patellofemoral dislocation. A tibiofemoral dislocation is a limb-threatening emergency due to the high rate of popliteal artery injury. The neurovascular bundle (popliteal artery, popliteal vein and common peroneal nerve) runs posteriorly in the popliteal fossa. The popliteal artery is tethered to the femur and tibia by a fibrous tunnel and is inherently immobile making it susceptible to injury during dislocation. Knee dislocations typically occur in major trauma. An MVC where the knee strikes the dashboard is a common scenario. The dislocation is usually clinically obvious and should be emergently reduced regardless of the presence of confirmatory X-rays. The leg should rapidly be assessed for any “hard” signs of vascular injury including an absence of pulse, limb ischemia, rapidly expanding hematoma, the presence of a bruit or thrill and pulsatile bleeding. Neurologic status should also be assessed prior to and after reduction. After reduction, all patients should have ankle-brachial index (ABI) performed. A normal ABI is > 0.9. Any patient with an ABI less than this should be further investigated for a popliteal injury with angiography. Splint and elevation (D) may be appropriate once a vascular injury is ruled out. The patient should not be discharged home (A) with an abnormal ABI. Observation and repeat ABI (B) is indicated if the initial ABI is normal.

PlayPlay

Episode 21 – Acute Kidney Injury

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

Dr. Josh Farkas of the PulmCrit blog has produced a couple of blog posts on the importance of renal protection in sepsis, Renoresuscitation: Sepsis resuscitation designed to avoid long-term complications and Renal microvascular hemodynamics in sepsis: a new paradigm.  Much of this is theoretical and certainly not something that is standard practice, rathery a theory extrapolated from subgroups of several trials.

Suggested renoresuscitation measures:

(1) Avoid renal failure – avoid nephrotoxins (many antibiotics, NSAIDs, ace-inhibitors), avoid hyperchloremic metabolic acidosis.

(2) Avoid volume overload – treating decreased urine output by flooding a patient with fluids is not necessarily the best move.

(3) Protect the glycocalyx of the endothelium – this suggestion proffers more questions than answers. Steroids? Albumin? Certain vasopressors?  Stay tuned, as we’re not really certain what this entails.

The Bread and Butter

We summarize some key topics from Rosenalli, that’s Tintinalli (7e) Chapter 91; Rosen’s (8e) Chapter 97.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Acute Kidney Injury – typically a creatinine 1.5-2x the patient’s baseline is classified as acute kidney injury.  Urine output can be increased initially but determine whether a patient is making urine and how much, as urine output <0.5 mL/kg/h qualifies as AKI.

RIFLE criteria
RIFLE criteria

Importance – AKI is associated with worse outcomes, although it’s unclear as to whether this is merely a marker of

  • Found in 35-65% of admissions to the intensive care unit, in 5-20% of hospital admissions.  Furthermore, AKI is associated with higher mortality.
  • Renal failure can also cause significant problems for the patient such as electrolyte abnormalities (hyperkalemia the most worriesome, but also hyperphosphatemia) and pulmonary edema.

Etiology – many causes of AKI are reversible or amenable to treatment.

Prerenal – this is one of the most common causes of acute kidney injury and basically is caused by decreased blood flow to the kidney.  Associated with a high BUN/creatinine ratio, increased urine osmolality, a urine sodium concentration less than 20 mEq/L, and FENa less than 1% (this is why getting urine sodium and a concurrent chemistry panel is key).

  • Hypovolemia – volume depleted, hemorrhage, intravascular volume depletion from congestive heart failure or cirrhosis.
  • Hypotension – poor cardiac output (heart failure, valvular problems), shock
  • Decreased flow through the renal artery disease – Nonsteroidal anti-inflammatories: inhibit prostaglandins in the afferent arteriole.  ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, leading to decreased levels of angiotensin II, which when absent decreases the GFR because of dilatation of the efferent arteriole.

Post Renal (Obstructive) – Check out Episode 2 on urologic emergencies.

  • Benign prostatic hypertrophy (BPH) is the most common cause but medications such as anticholinergics and pseudoephedrine. Trauma, stones, strictures, and malignancy can also cause obstruction.

Intrinsic acute renal failure divided into: tubular disease (most common), glomerular disease, vascular disease and interstitial disease.

  • Least common form of AKI in the ED, more common in inpatients.
  • Acute Tubular Necrosis (ATN) most common cause – via nephrotoxins such as aminoglycosides and contrast.
  • Granular “muddy brown” casts – think of necrosis from the “N” in ATN and necrosis tends to be dark.

Indications for emergent dialysis – AEIOU

A- Acidosis

E- Electrolyte emergencies (hyperkalemia!)

I-  Intoxication with dialyzable toxins (ethylene glycol)

O- Overloaded with volume

U- Uremia

 Generously Donated Rosh Review Questions 

Question 1. A 72-year-old man is brought to the ED from a nursing home for evaluation of oliguria. He is found to have an acutely elevated BUN and plasma creatinine from baseline. A Foley catheter is placed; his urine sodium (UNa) is measured below 20 mEq/L and fractional excretion of sodium (FENa) below 1%. [polldaddy poll=8545511]

Question 2.  A 54-year-old man presents to the ED in acute renal failure (ARF). [polldaddy poll=8545512]

Answer 1.  D. This patient’s oliguria with acutely elevated BUN and plasma creatinine suggest that he is in acute renal failure (ARF). His UNa <20 mEq/L and FENa <1% indicate that he has intact reabsorptive function and is able to conserve sodium. This is consistent with prerenal azotemia as the cause for his ARF.

Acute tubular necrosis (ATN) (A), loop diuretics (e.g., furosemide) (B), and osmotic diuresis (e.g., mannitol) (C)all lead to UNa >20 mEq/L and FENa >1% because there is impairment in the ability to concentrate the urine. In such cases, a high-sodium load is excreted.

Answer 2. A.   Acute tubular necrosis (ATN) is a severe form of impairment of tubular epithelial cells caused by ischemia or toxic injury. It is a leading cause of ARF. One of its hallmarks is the presence of brown granular casts on urinalysis. These contain cellular debris rich in cytochrome pigments. In contrast, hyaline casts (B) are usually nonspecific but present after exercise; red cell casts (C) are indicative of glomerular hematuria (e.g., glomerulonephritis); and white cell casts (D) imply renal parenchymal inflammation (e.g., acute interstitial nephritis, pyelonephritis).

Episode 19 – Environment: Mushrooms and Hypothermia

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

We review the Tox Talk podcast, Episode 23 – Mushrooms.  Our favorite pearls:

Clitocybe, Inocybe – contain muscarine which stimulates muscarinic receptors (acetylcholine/parasympathetic), causing a cholinergic toxidrome. Think SLUDGE (salivation, lacrimation, urination, defecation, gastric emptying/emesis) and the Killer B’s (bradycardia, bronchorrhea, bronchospasm) or DUMBELLS (diarrhea/diaphoresis, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation). Basically, cholinergic toxidrome: SMALL, WET, SLOW.

  • Memory aid: these mushrooms end in -yBE, akin to the “killer B’s” that make cholinergic toxicity deadly.

Gyromitra – (false morel) contains gyromitrin which can cause seizures, in addition to gastrointestinal upset and liver failure.  Treatment: pyridoxine (B6).

  • Memory aid: gyromitra named because they look like the gyri of the brain and, conveniently, make the brain seize through depletion of GABA.

Amanita phalloides – contains amatoxins which cause delayed gastrointestinal symptoms and liver failure., echoing acetaminophen toxicity.

  • Caution: this is different than the amanita muscaria ‘mushroom, which is tricky because that amanita muscaria has neither muscarinic properties nor the toxicity of amanita phalloides.

Bonus pearl: Coprinus species can cause a disulfiram like reaction.

FOAM article on mushrooms by Jo et al

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter  ; Rosen’s 8(e) Chapter  – but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Hypothermia starts at 35°C and then is categorized based on severity.

Pearls:

  • Ethanol + hypothermia = bad news.  Ethanol is the most common cause of excessive heat loss in urban areas as people tend to not take warming measures, may be homeless or without heat, and have impaired thermoregulation.  Hypothermia also slows alcohol metabolism, making people drunker for longer.
  • Elderly patients are more susceptible to hypothermia, particularly as they may not sense the cooler temperatures.  Some may also have impaired thermoregulation.
  • Have a low threshold

Diagnostics:

  • Get a temperature, on all patients.  This applies to patient’s “found down” as well as the chronic alcoholic who just seems really drunk.
  • If patients aren’t rewarming 1°C/hr and they’re above 32°C, consider: sepsis, cortisol deficiency, myxedema, ethanol.
  • The J wave or “Osborn” wave is found in many cases of hypothermia, often quoted at ~80%.  However, it is not pathognomonic for hypothermia.
From the Rosh Review

Treatment: Warm the patient.  Don’t call the patient dead until they’re warm and dead, which means their temp is above 30-32°C.

Screen Shot 2014-11-22 at 9.30.13 PM

Passive Rewarming – effective when the patient can still shiver (33-35°C).

  • Generates ~1.5°C of heat/hr

Active Rewarming – direct transfer of heat to the patient.

  • Indications: Cardiovascular instability, temp ≤30-32° C, inadequate rate of rewarming or failure to rewarm, endocrine problem, trauma, tox, secondary hypothermia impairing thermoregulation
  • Can be external or internal (which can be minimally invasive like IV fluids or quite invasive with things like bypass or pleural lavage).

Outcomes

  • Unlikely survival with a potassium > 12 mmol/L and recommendations are to terminate resuscitation for potassium >12 mmol/L and consider cessation for potassium between 10-12 mmol/L

FOAM Resources:

EBM Gone Wild on Prognostication

ScanCrit on ECMO in Accidental Hypothermia

EMCrit on Severe Accidental Hypothermia

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  A 40-year-old man with a history of substance abuse is brought in by EMS after being found unconscious outside of a nightclub in the middle of winter. It is unclear how long he was outside. He is unresponsive with a GCS of 3.[polldaddy poll=8469565]

Question 2.  What is the most common cause of death in hypothermic patients after successful resuscitation?

Question 3.

[polldaddy poll=8473489]

Question 4. What abnormal rhythm is common with temperatures below 32°C?

References:

Danzl DF, Zafren K. Accidental Hypothermia, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2013, (Ch) 140: pp 1883-1885.

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

Mair P, Kornberger E, et al. Prognostic markers in patients with severe accidental hypothermia and cardiocirculatory arrest. Resuscitation 1994;27:47-54.

Answers:

1. D. When the serum potassium is greater than 12 mmol/L resuscitative efforts should be halted as the patient is unlikely to survive and further efforts constitute futile care. Accidental hypothermia is not an uncommon occurrence particularly in colder climates. It may occur in conjunction with substance abuse when an individual becomes impaired and is subsequently exposed to the outdoors. It can also occur as a result of drowning, avalanche and other trauma. Bio-makers other than potassium have been studied including serum lactate (B), pH (C) and clotting time. None have been proven prognostically reliable and therefore should not be used as a guide to determine if resuscitation should be continued. Hypothermic patients that present in cardiac arrest should be warmed to a minimum of 32°C (A) preferably via ECMO or cardiopulmonary bypass. However, if a hypothermic patient is warmed to 32°C and remains in asystole, recovery is unlikely and resuscitative efforts should be terminated. Other indications to cease resuscitative efforts include: obvious signs of irreversible death (e.g. major trauma), valid DNR order, conditions that are unsafe for the rescuer or provider, and an avalanche burial > 35 minutes in which the airway is packed with snow and the patient is asystolic.

2. Pulmonary edema.

2. C. Hypothermia. The ECG demonstrates the presence of J waves or Osborn waves which are seen in hypothermia. One of the first cardiac effects of hypothermia is bradycardia secondary to decreased firing of the cardiac pacemaker cells in cold temperatures. Osborn waves may appear at any temperature below 32°C. The waves are an upward deflection at the terminal portion of the QRS complex. They may represent abnormal ion flux in cold temperatures along with delayed depolarization and early repolarization of the left ventricular wall. As temperatures continue to drop, the ECG will demonstrate prolonged intervals: PR, followed by QRS and then QTc. Both diabetic ketoacidosis (A) and digoxin toxicity (B) may lead to hyperkalemia. In diabetic ketoacidosis, hyperkalemia develops as a result of the acidic pH in the blood and the transport of hydrogen ions intracellularly in exchange for a potassium ion. Digoxin toxicity poisons the cellular Na+/K+ ATPase resulting in elevated extracellular levels of potassium. The ECG manifestations of hyperkalemia begin with peaked T waves. Multiple other findings eventually develop including a shortened QT interval, ST depression, bundle branch blocks, widened QRS, prolonged PR interval, flattened T wave and ultimately a sine wave. Hyperparathyroidism (D) may lead to hypercalcemia. In hypercalcemia, the ECG shows a shortened QT interval, flattened T waves and QRS widening at very high levels.

4.  Atrial fibrillation.

PlayPlay