NNT of 8 for excellent functional outcomes; 95% [CI] 4-31
Paucity of patients presenting with mild stroke (NIHSS score 0 to 4)
NNH of 17 for symptomatic intracerebral hemorrhage; 95% CI 12-34
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 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.
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]
We are bringing you pearls from conferences we attend including SMACC (#smaccUS). The plenary, facilitated by the brilliant Dr. Victoria Brazil, focused on the impaired provider. At SMACC we’ve heard time and time again – we are fallible, we make mistakes.
Dying – Dr. Ashley Shreves
What often presume what our patients want without asking them. When dying patients are asked what they want, it comes down to dignity. 1) Being clean 2) Naming a decision maker and then other top priorities essentially come down to healthcare providers listening [Steinhauser et al]
We don’t ask patients about their code statuses appropriately. First, we often spend almost no time doing this. One study of hospitalists found that code status discussions lasted, on average, one minute. Further, that one minute was spent mostly focused on procedures [Anderson et al]
Communicate!
Evidence Based Medicine – The consensus of these cage matches was that evidence isn’t all equal; the existence of data doesn’t necessarily mean it’s good data.
The Randomized Control Trial (RCT) has problems – Drs. Paul Young and Simon Finfer
Caution with Base Rate Neglect – we jump to inappropriate conclusions. For example, pretend you have tested positive for a typically fatal disease. The test is accurate 95% of the time. Most people would conclude that there was a 95% chance they have the disease – a death sentence. Yet, one would need to know the prevalence of the disease in the general population to determine the actual likelihood that the test was correct. If the prevalence of the disease is 1 in 1000, the likelihood that you actually have the disease based on this test is <2%.
We should read the primary literature, but we can’t read all of it. Use FOAM (judiciously) – Drs. Rory Spiegel and Ken Milne
Due to the volume of literature, we have to make some decisions on what to read (Systematic reviews? Meta-analyses? RCTs? Case Reports?)
Severe traumatic brain injury can cause apnea which leads to a spiral of hypoxia (and thus cell death) and hypercapnea (with cerebral vasodilation causing cerebral edema) which can result in poor neurologic outcome.
The key? Resuscitate these patients as a hypoxic arrest. These are patients that need an airway and need oxygen.
We are bringing you pearls from conferences we attend including SMACC (#smaccUS). The overarching theme to Day 1 at SMACC? Use your team- to keep you in check and for feedback. Our cases and errors are opportunities for reflection. Dr. Cliff Reid reminded us to follow up our patients and outcomes and learn from it all, without letting our egos get in the way. Dr. Simon Carley (St. Emlyn’s) gave a powerful talk on learning from mistakes later in the day; you will definitely want to listen to these when they come out.
The sub theme? Experts don’t need algorithms and tests. But the novices? That’s another story.
Trauma – Weingart. We won’t delve into his thoughts on ATLS here (hint: ATLS isn’t for experts).
Ignore the first automated blood pressure, it’s probably wrong. Get a manual blood pressure.
Giving 3 units of blood in one hour? Prepare for massive transfusion, that means FFP, platelets, everything
If you go down the massive transfusion pathways, give an ampule of calcium every 4-6 units of plasma to combat the transfusion induced hypocalcemia from citrate.
The Shock Index (HR/SBP), isn’t as exciting as we once thought. It may be a guide, but not reliably so.
Pain – Strayer
Analgesia doesn’t = opiates. Think about local analgesia.
Pain as the “5th vital sign” – probably more harmful than helpful [Gussow]
In fact, in 2009, there were
Polypharmacy – Juurlink
Trimethoprim/sulfamethoxazole and ace-inhibitors/angiotensin receptor blockers, used in combination can lead to hyperkalemia and, in some cases, death [Juurlink et al]
Acetaminophen, at just 2 grams/day, can elevate the INR in patients on warfarin [Pinson]. Acetaminophen is still probably the analgesic of choice, but something to be aware of
Sepsis
Lactate is not a measure of tissue hypoxia/anaerobic metabolism [Marik et al]
Too much fluid is not a good thing = iatrogenic salt water drowning [Marik et al]
Patients may need vasopressors. If they do, don’t delay based on central access. Vasopressors are ok through good peripheral lines for a day or so. [Loubani et al, Mayo et al] However, we should probably place the lines when we’re safely able.
Of note, this does require strict protocols. Ex: Mayo study had stringent inclusion criteria
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
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.
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.
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].
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).
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:
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.
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.
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.
Diabetic Emergencies : New Strategies For An Old Disease.
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.
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.
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.
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.
We enjoy contributing to the Free Open Access Medical education (FOAM) community. Creating FOAM is not free and requires significant costs in time and money. Yet, we find this investment invaluable and appreciate everyone who listens, as well as those who champion our endeavor (including the supportive people in our life that tolerate “FOAMcast dates” and tiptoe around whilst recording). We would also like to thank everyone who has contributed by means of post-publication peer review (Brett Schupack, Dr. Marc Probst, Dr. Gabriel Cade, Dr. Iain Beardsell, and countless others). Please continue to not only let us know when we get it right, but also when we get it wrong. We appreciate the suggestions, praise, feedback, and corrections.
Given our love of spaced repetition, we review our favorite pearls and mnemonics from the past year.
HANG IV: hernia, adhesions, neoplasm, gallstone (ileus), intussception,
Heart failure episode – treatment for right ventricular heart failure.
Optimize OHCRAP – Oxygenation, Hemodynamics, Contractility, Rate/rhythm, Afterload, and Preload
Headaches – Likelihood of migraine diagnosis (comes from the outpatient literature) = POUND. 4 criteria very indicative of migraine (+LR 24), 3 criteria also likely (+LR 3)
Pounding headache
hOurs: headache lasts 4-72 h without medication
Unilateral headaches
Nausea
Disabling: disrupts daily activities
Our most frequently used clinical pearl:
The hand exam, in one movement:
Motor Exam of the Hand
Our favorite visual aid:
Burns – Grading the burn according to the Egyptian flag (because we all knew what that looked like).
Burn Degree
Worst visual aid: the Knee volcano (we won’t go there again)
Cord – complete cord syndrome that persists longer than 24 hours is highly unlikely to have any motor recovery. These patients need urgent intervention. This is we must differentiate between the complete and incomplete cord syndromes. Complete = “total loss of motor power and sensation distal to the site of the spinal injury.”
Knee/Leg– Beware knee dislocations. Of patients with popliteal disruption, the amputation rate rises to 90% 8 hours after the injury without surgical intervention.
Knee Dislocation Algorithm
Time is skin?
Hey Jeremy, re burns – surely needed a ‘Time is skin’?? @FOAMpodcast
Malignant hyperthermia – a rare condition typically associated with volatile anesthetics, so more often an OR/inpatient issue; however, has been associated with succinylcholine use.
Cause: most often a mutation of the ryanodine receptor which, in the presence of certain anesthetics or succinylcholine causes too much intracellular calcium. This leads to increased ATP production.
Caution with calcium channel blockers – may lead to hyperkalemia or myocardial depression
Dantrolene has also been used in severe dinitrophenol (industrial chemical and weight loss supplement) toxicity – see this Poison Review post.
The Bread and Butter
We cover syndromes associated with psychiatric medications and polypharmacy including neuroleptic malignant syndrome (NMS), serotonin syndrome, and some extrapyramidal side effects. We do this based on Rosen’s Emergency and Tintinalli. But, don’t just take our word for it. Go enrich your fundamental understanding yourself.
Ref: Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352:(11)1112-20.
Neuroleptic Malignant Syndrome
Caused by atypical antipsychotics, rare, idiosyncratic and may persist for 2+ weeks after discontinuation of the offending medication
Symptoms – Varied diagnostic criteria but requires temp >100.4F + muscle rigidity + at least two of the following (in rough order of frequency):
Diaphoresis
Leukocytosis
AMS
Elevated creatine kinase
Labile blood pressure
Tachycardia
Tremor
Incontinence
Dysphagia
Mutism
Treatment – remove offending agents, supportive care (intravenous fluids, cooling), benzodiazepines. Dantrolene, amantadine, and bromocriptine are not recommended.
Serotonin Syndrome
(PV card from Academic Life in Emergency Medicine). Caution with the elderly as these symptoms may be attributed to infection or delirium (and vice versa).
Symptoms – Classical clinical triad of AMS + Autonomic instability (Hyperthermia, Tachycardia, diaphoresis) + Neuromuscular Abnormalities: Myoclonus, ocular clonus, rigidity, hyperreflexia, tremor. Yet like most clinical triads, this performs poorly. The Hunter Criteria are often used (Sensitivity ~84%):
Serotonergic agent plus 1 of the following:
Spontaneous clonus
Inducible clonus + agitation or diaphoresis
Ocular Clonus + agitation or diaphoresis
Tremor + hyperreflexia
Hypertonia + temp >38F AND ocular clonus or inducible clonus
Serotonin syndrome often begins with akathisia (restlessness) and body systems become increasingly “ramped up” with tremors, followed by altered mental status, and then incereasing amounts of rigidity (inducible clonus -> Sustained clonus (+/- ocular clonus) -> Muscular rigidity -> Hyperthermia -> Death)
Causes – While often associated with antidepressants, polypharmacy seems to be the culprit here. Serotonin syndrome is commonly associated with some of these medications
Question 1. A 35-year-old man presents with fever, hypertension and altered mental status. He was recently started on haloperidol for schizophrenia. Physical examination reveals a confused patient with muscle rigidity. [polldaddy poll=8842561]
Answers
1. C. FOAMcast editorial: This is an exercise in selecting the *best* answer, not the one that is most correct. You’ve probably noted that a benzodiazepine is not an option, the next best option is dantrolene.
This patient presents with signs and symptoms concerning for neuroleptic malignant syndrome (NMS) and should be treated with dantrolene. NMS is a life-threatening complication of neuroleptic drug treatment. It is rare and only effects 0.5 – 1% of patients receiving these drugs. Although it is more common with use of the typical neuroleptic medications, it can also be seen with the atypical agents. It usually occurs within the first few weeks of starting neuroleptic medications but can also be seen after an increase in dosage. NMS is characterized bymuscle rigidity, fever, altered mental status and autonomic instability. Muscle contraction leads to an elevated serum creatinine kinase. Due to similarities, the disease may be confused with serotonin syndrome. NMS can become complicated by respiratory, hepatic or renal failure, cardiovascular collapse, coagulopathy or gastrointestinal hemorrhage. Dantrolene is a direct acting muscle relaxant that can be beneficial in severe cases.
Temperature – often causing burns down to the level of the vocal cords, but not below.
Toxins – products of combustion such as cyanide, carbon monoxide, and hydrogen sulfide are asphyxiants and impair oxygen utilization
Irritants – inhaled particulates irritate airways
Airway edema peaks at 24-48 hours
Diagnosis made on bronchoscopy
Nebulized heparin, N-acetylcysteine, and albuterol protocol
May be beneficial, but protocols based on small studies. Rosen gives a head nod to this regimen, yet the evidence is questionable [1-3].
Nebulized heparin can be used at 10,000 international units every 4 hours, followed by nebulized NAC & albuterol 2 hours later for a total of 7 days.
Nebulized heparin may help prevent formation of airways casts.
NAC may have a mucolytic effect and help scavenge free radicals.
Albuterol added to prevent bronchospasm
Alternating nebulized heparin and NAC may:
Improve P/F ratio (not a patient centered outcome)
Decrease ventilator days
Reduce the development of acute lung injury
The Bread and Butter
We cover burns including nomenclature, fluid resuscitation, burn center referral criteria, and more. We do this based on Rosen’s and Tintinalli. But, don’t just take our word for it. Go enrich your fundamental understanding yourself.
Burn Depth
Classically, burns were described in degrees but are now described by the degree of thickness (except, apparently, fourth degree burns). At FOAMcast, we like to remember these distinctions by thinking about the Egyptian flag, with the flag pole representing fourth degree burn or burns essentially down to the bone.
Burn Degree
Fluid Resuscitation
The Parkland Formula is probably one of the most well known but both this formula and the modified Brooke formula have led to fluid “creep” or over-resuscitation, which may have lasting consequences. Major guidelines and Rosenalli approve another method, the “Rule of Tens.”
Question 2. A 52-year-old woman is brought to the emergency department with burns from a house fire. Physical exam reveals superficial burns over her entire left arm and partial-thickness and full-thickness burns covering her entire right arm, her anterior right leg and anterior trunk. [polldaddy poll=8824315]
Answers
1. C. Burn classification is based on burn depth. Second-degree burns are classified into superficial and deep partial-thickness burns. Deep partial-thickness burns extend into thereticular dermis. Skin color is usually a mixture of red and blanched white, and capillary refill is slow. Blisters are thick-walled and commonly ruptured and the skin may appear leathery white. Two-point discrimination may be diminished, but pressure and pinprick applied to the burned skin can be felt. Whereas superficial partial-thickness burns usually re-epithelialize 7-10 days after injury; so the risk of hypertrophic scarring is very small. For deep partial-thickness burns, tissue may undergo spontaneous epithelialization from the few viable epithelial appendages at this deepest layer of dermis and heal within 3-6 weeks. Because these burns have less capacity for re-epithelializing, a greater potential for hypertrophic scar formation exists. In deep partial-thickness burns, treatment with topical antimicrobial dressings is necessary to prevent infection as the burn wound heals. Contraction across joints, with resulting limitation in range of motion, is a common sequela. Splash scalds often cause second-degree burns.
2. B. The extent of burn size in this patient is 36% total body surface area. A thorough and accurate estimation of burn size is essential to guide therapy and to determine when to transfer a patient to a burn center. The extent of burns is expressed as the total percentage of body surface area. Superficial burns are not included in the burn assessment. For adult assessment, the most expeditious method to estimate total percentage of body surface area is the Rule of Nines. This method only takes into account partial-thickness and full-thickness burns. Each leg represents 18% total percentage of body surface area; each arm represents 9% total percentage of body surface area; the anterior and posterior trunk each represent 18% total percentage of body surface area; and the head represents 9% total percentage of body surface area. This patient has partial-thickness and full-thickness burns covering her entire right arm, her anterior right leg and anterior trunk, which calculates to 36%. The superficial burn on her left arm is not included in the calculation. According to the Rule of Nines, the percentage in this patient can be calculated as follows: entire right arm = 9%; anterior right leg = 9%; anterior trunk 18%. 9+9+18= 36%.
2. Kashefi NS, Nathan JI, Dissanaike S. Does a Nebulized Heparin/N-acetylcysteine Protocol Improve Outcomes in Adult Smoke Inhalation? Plast Reconstr Surg Glob Open. 2014;2:(6)e165. [pubmed]
3. Elsharnouby NM, Eid HE, Abou Elezz NF, Aboelatta YA. Heparin/N-acetylcysteine: an adjuvant in the management of burn inhalation injury: a study of different doses. J Crit Care. 2014;29:(1)182.e1-4. [pubmed]
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.”
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)
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.
