UMEM Educational Pearls

Some common injuries and their board review associated complications

• Anterior Shoulder Dislocation = Axillary nerve or artery injury
• Supracondylar Fracture = Brachial Artery injury
• Posterior Elbow Dislocation = Brachial Artery injury
• Knee Dislocation = Popiteal Artery Injury and Peroneal and tibial nerve injury
• Humeral shaft fracture = radial nerve injury
• Posterior hip dislocation = sciatica nerve injury
• Anterior hip dislocation = femoral nerve injury

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Pediatric Ethanol Ingestion

A young child is brought to you after accidentally drinking a shot of alcohol at a wedding party. Here is what you need to consider:

• Infants and young children who have ingested enough ethanol to cause a peak serum level ≥50 mg/dL (11 mmol/L) are at risk for profound hypoglycemia, in addition to the other effects of alcohol seen in adults The key is that the dangerous serum level is MUCH lower in children than in adults, and children require FAR smaller volume than what may be considered dangerous by adults.
• Supportive care is the key to good outcomes, with particular focus on treating hypoglycemia - check your D-sticks early and often.
• Consider child protective services involvement in every case of pediatric intoxication, and consider measurement of serum acetaminophen levels as well as other possible toxic ingestion candidates.
• Activated charcoal cannot adsorb ethanol and should only be used if other substances are being considered.
• Children who are asymptomatic for six hours, and have a safe home environment, may be discharged.

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The number of rabies vaccines recommended by the ACIP (Advisory Committee on Immunization Practices) has been reduced from 5 to 4 doses for unvaccinated patients.

This was based on evidence from multiple source, including pathogenesis data, animal trials, clinical studies, and epidemiological surveillance. The first dose of the 4-dose regimen should be administered as soon as possible after exposure (day 0). Additional doses are then given on day 3, 7, and 14. The first dose of rabies vaccine should be administered with HRIG, infiltrating as much as possible into the wound, with the remainder given IM at a distant site from the vaccine.

This recommendation is not applicable to immunocompromised patients, who should continue to receive the full five doses.

http://www.cdc.gov/vaccines/pubs/vis/downloads/vis-rabies.pdf

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Cluster headaches are defined as a group of at least five headache attacks causing unilateral orbital, supraorbital and/or temporal pain, with at least one of the following simultaneous associated findings on the affected side:

1. conjunctival injection
2. lacrimation
3. nasal congestion
4. rhinorrhea
5. ptosis
6. miosis
7. sweating on the forehead

Cluster headaches can occur at a frequency of one every other day t  eight episodes per day.

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Hypocapnia and Brain Injury

• Hypocapnia indirectly reduces cerebral blood volume through reductions in arterial cerebral blood flow.
• Despite its continued and frequent use, hypocapnia can actually aggravate cerebral hypoxia through reductions in oxygen supply and increases in cerebral oxygen demand.
• In addition to inducing further cerebral injury, hypocapnia can cause deleterious effects on the heart, lung, and GI tract.
• To date, there is no evidence that hypocapnia improves outcome in patients with traumatic brain injury or acute stroke.
• Induced hypocapnia in critically ill ED patients with acute brain injury should primarily be reserved for those with imminent brain herniation.

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Pulmonary Embolism and Blood Pressure

Patients with massive PE will often develop worsening hypotension after a fluid bolus due to increased right ventricular distension and deviation of the interventricular septum towards the left side of the heart. This septal deviation decreases left heart cardiac output.

In addition, patients with massive PE will sometimes develop higher blood pressures after intubation as positive pressure ventilation reduces preload, decreases deviation of the septum, and increases left sided cardiac output.

Diabetic Ketoacidosis Treatment:

• At least at our academic medical center, we find it very hard to get a DKA patient admitted to an ICU or IMC while they are still in DKA.  Typically, we can correct the acidosis and downgrade them to a floor bed before their ICU/IMC bed is available.
• Some key points to remember when managing DKA in the ED.
  • The mainstay of treatment for the hyperglycemia initially is IV fluids.
  • Check labs often and replete Magnesium and Potassium early.
  • Insulin should not be started until the potassium is confirmed to be >3.3 mEq/L
  • Patients can still be in DKA even though there glucose is normal.
  • Intravenous insulin must be continued until all the ketones are cleared. 
  • Add D5W or D10 if needed to ensure that their glucose levels stay up but do not stop the insulin.
  • Patients need to receive a long acting insulin (i.e.: Lantus or NPH) 2 hours before the insulin drip is stopped.  Placing a patient only on Sliding Scale Insulin will almost guarantee that they go back into DKA on the floor.
  • Typically you can just restart the patients home long acting insulin, but if you are leary about hypoglycemia if they are not eating well, then give them 3/4 their home dose.

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• newborns have increased rates of bilirubin production due to RBC's with shorter life spans, and a decreased rate of bilirubin elimination due to decreased ability of the neonatal liver to conjugate bilirubin
• about 60% of newborns will become clinically jaundiced
• bilirubin levels peat at 4 days of life,  and may not decline before day 7
• admission and treatment should be considered urgently when serum total bilirubin >25mg/dL, with exchange transfusion if it is >30mg/dL or the infant has signs of kernicterus
• there are nomograms which plot the bilirubin level according to the infant's age in hours to determine if an infant is at risk for being at toxic levels
• the most common pathologic etiologies are due to increased bilirubin production: blood-group incompatibilities, RBC-enzyme deficiency, and RBC structural defects
• when jaundice occurs between days 4-7, strongly consider sepsis, UTI, congenital infection (syphilis, CMV, etc)

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Ingestion of caustics can lead to immediate burns to mouth, esophagus, stomach as well as possible perforation. Months and years later, further complications are esophageal stenosis and increased incidence of esophageal carcinoma. The main benefit to EGD is to determine extent of injury within the esophagus. The lesions are graded much like a burn: 

Grade I: Mild burn, no risk for esophageal stenosis

Grade II: Moderate, if circumferential, patient is at risk for esophageal stenosis

Grade II: Eschar present, high risk of perforation as well as esophagel stenosis

You can make a case that all intentional-suicidal ingestions of caustics should undergo EGD since there should be some injury if ingestion truly occurred or at the least a higher probability. The difficult case is the pediatric unintentional ingestion. Utilizing clinical exam and history will assist with that determination - there is a little research to guide this decision (next pearl)

The attached picture is the post-mortem of a caustic injury showing grade II linear lesions in esophagus with eschar distally and in stomach (Grade III).

Migraine with aura (MA) diagnostic criteria

A. At least two attacks with at least 3 of the following:

1. One or more fully reversible aura symptoms (indicates focal cerebral cortical and/or brain stem functions).

2. At least 1 aura symptom develops gradually over greater than 4 minutes, or 2 or more symptoms occur in succession.

3. No aura symptom lasts greater than 60 minutes.

4. Headache follows aura with free interval of at least 60 minutes.

B. At least 1 of the following aura features establishes a diagnosis of migraine with typical aura:

1. Homonymous visual disturbance.

2. Unilateral paresthesias and/or numbness.

3. Unilateral weakness.

4. Aphasia or speech difficulty.

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Drug-Induced Thrombocytopenia

• Thrombocytopenia is common in critically ill patients and is associated with increased mortality.
• Up to 25% of critically ill patients will develop thrombocytopenia as a result of a medication, termed drug-induced thrombocytopenia (DIT)
• Antibiotcs are a common, yet infrequently recognized, cause of DIT.
• Antibiotics reported to cause DIT include linezolid, vancomycin, trimethoprim/sulfamethoxazole, and the beta-lactams.
• In fact, piperacillin/tazobactam has been associated with DIT more frequently than any other penicillin. 

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Classic electrocardiographic findings for hypokalemia:
u-waves (produces appearance of long QT), especially in the precordial leads
ventricular ectopy (PVCs typically)
ST segment depression or downward sagging, especially in the precordial leads

note that the sagging ST segments that terminate in large U-waves end up producing biphasic T-waves; these have the mirror image appearance of Wellens waves

• Back pain is the most common musculoskeletal complaint that results in visits to the ED.
• It has a benign course in more than 90% of patients, so we must be vigilant and comfortable looking for warning signs of a neurologically impairing or life-threatening cause.
• We rely on the presence of so-called "red flags" or alarm symptoms to guide further diagnostic tests, specialty evaluation, and treatment. 
• Additionally, always consider 2 important extra-spinal causes of back pain: aortic dissection (sudden onset back pain) and abdominal aortic aneurysm (patients >50, esp. those who you think have a kidney stone- isolated back and groin pain is a common presentation).

A patient arrives via EMS agitated with VS: P 140, BP 155/100, R 18, T 101F. There is an admitted drug exposure and you examine his eyes which are dilated. You shine the light in the eyes - if the pupil reacts, would that be consistent with anticholinergic or sympathomimetic toxidrome?

Answer: Anticholinergic exposure paralyzes pupillary constrictor muscles and causes dilated pupils that do not react to light. Think about when you go to the eye doctor's office. They put homoatropine in your eyes so that when they look with the slit lamp they can see the retina without interference from pupillary constriction. Sympathomimetic exposure like cocaine activates pupillary dilator muscles, the constrictors are still intact and will give a reflexive constriction to light.  This patient has reactive pupils and by the mere fact is in Baltimore probability dictates a sympathomimetic exposure like cocaine.

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• Several medications such as dopamine-blocking anti-emetics, triptans, and ergotamine derivatives have been shown to more effectively treat migraine headaches over other types of headaches, making the ability to accurately recognize this common (2.2% of all ED visits) condition essential.

• According to the International Headache Society, one meets diagnostic criteria for migraine headache without aura when they have experienced at least 5 attacks, each lasting 4 to 72 hours (untreated or unsuccessfully treated) and accompanied by at least 2 of the 4 following characteristics ("PUMA"):

          A.

              1.  Pulsatile or throbbing in quality

              2.  Unilateral in location

              3.  Moderate to severe in intensity

              4.  Aggravated by activity (i.e.climbing stairs, exertion), plus

         B.  at least 1 of the following 2 during the headache  ("VP"): 

              1.  Vomiting and/or nausea

              2.  Photophobia and/or phonophobia

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ICU Acquired Weakness

• ICU acquired weakness (ICU-aw) is a general term that refers to the weakness that develops in critically ill patients during the course of their illness - especially in patients with sepsis and those receiving mechanical ventilation.
• ICU-aw is an very common complication of critical illness that can develop within hours and has been shown to increase the duration of mechanical ventilation and ICU/hospital LOS.  Observational studies have also reported an association with mortality.
• Risk factors associated with ICU-aw include medications (neuromuscular blocking agents, corticosteroids), hyperglycemia and immobility.
• For the critically ill ED patient, current recommendations suggest limiting the administration of neuromuscular blocking agents and corticosteroids, when possible.

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There are multiple reasons for ST-segment elevation, the most important of which is acute myocardial infarction. However, because the treatment difference between MI vs. other more benign causes is so important, one should keep in mind the following factors that strongly point toward the diagnosis of MI:
1. the presence of ST-segment depression in any lead aside from aVR or V1
2. ST elevation that is horizontal or convex upwards (like a tombstone)
3. ST or T-wave morphologies that change over time with serial testing
4. ST changes compared to old ECGs
5. the development of Q-waves
6. ST elevation that follows coronary anatomy (e.g. limited to inferior leads, anterior leads, or lateral leads)

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The Salter Harris  Classification System is used in pediatric epiphyseal fractures.  The higher the type of fracture the poorer the prognosis

Some common exam facts about Salter Harris Fractures are:

1. The type II fracture is the most common.
2. The small metaphyseal fragment in Salter Harris type II and IV fractures is called the Thurston Holland Sign.
3. Type III and IV fractures often require open reduction and internal fracture due to the fracture extending into the joint.
4. Type V fractures may appear normal, but the epiphyseal plate is crushed and the blood supply is interrupted.

The Classification system as listed by Type:

• Type I: A fracture through the physeal growth plate. Typically can not be seen on x-ray unless they growth plate is widened.
• Type II: A fracture through the physeal growth plate and metaphysis.
• Type III: A fracture through the physeal growth plate and epiphysis.
• Type IV: A fracture through the physis, physeal growth plate and metaphysis.
• Type V: A crush injury of the physeal growth plate.

A image of the fractures can be found on FP Notebook at http://www.fpnotebook.com/_media/OrthoFractureSalterHarris.jpg

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Valproic Acid (Depakote) is a drug that uniquely has the ability to raise serum ammonia concentrations. It is able to do this without raising liver er enzymes and it can occur in overdose or at therapeutic levels. Do not think of this in the context of hepatic encephalopathy. This a metabolic derangement caused by VPA.

• Any patient with somnolence, lethargy, decreased responsiveness - order a serum ammonia level as well as Valproic acid level
• If the serum ammonia is elevated in conjunction with altered mental status consider a trial of carnitine
• L-carnitine is a safe drug that is used in nutritional supplementation. VPA and other anticonvulsants cause carnitine deficiency
• Most effective dose is unknown but from a recent review: IV 100 mg/kg once, followed by infusions of 50 mg/kg (to a maximum of 3 g per dose) every 8 hours until patient improves, ammonia decreases

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  Perrott J, Murphy NG, Zed PJ. L-carnitine for acute valproic Acid overdose: a   systematic review of published cases. Ann Pharmacother. 2010  Jul-Aug;44(7-8):1287-93. Epub 2010 Jun 29.

• Lacunar infarcts affect the deep penetrating vessels of the middle cerebral artery and carry the best prognosis of all strokes.

• There are 4 classic syndromes characteristically caused by lacunar infarcts, with which the emergency physician should be familiar and able to recognize.  They are:

1. Pure motor hemiparesis.
2. Pure sensory syndrome.
3. Ataxic hemiparesis (ipsilateral cerebellar and motor symptoms).
4. Clumsy hand dysarthria syndrome (ipsilateral hand weakness, patient may say their hand "feels awkward," dysarthria more pronounced than the weakness).