At the end of every year, the Intennal Medicine residency at Hennepin County Medical Center holds a poster session for the graduating senior residents. Each resident is encouraged to display work from their time during residency. Most residents prepare a poster on research they worked on or quality improvement projects. Others have shown off education innovations they came up with, or simulation cases they developed.

I enjoy sketching/drawing and have prepared many figures for the presentations, papers, lectures, blog posts, and teaching that I have done during my residency. I thought it would be fun and unique to prepare a poster with a sample of my art. Nothing earth shattering, but I hope you enjoy.

Tissue plasminogen activator (tPA, trade-name alteplase) catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown. Its fibrinolysis properties makes it clinically useful for treatment of treatment of myocardial infarction with ST-elevation (STEMI), acute ischemic emboilc or thrombotic stroke (AIS), acute massive pulmonary embolism, and central venous access devices (CVAD). Alteplase is produced by Genentech, and is manufactured using recombinant biotechnology techniques. Other r-tPA medications are Reteplase and Tenecteplase.

Unfortunately these medications are not used daily, and often in emergent situations. For facilities without 24-hours pharmacy coverage, it is often left to the nursing staff or physician to prepare the medication. The preparation instructions included in the kit are complicated, and you should be familiar with the procedure before the need arises. In this tutorial I will walk you through the mixing procedure.

Step 1

When you the open the kit you will find a vial of sterile normal saline and a sterile vial of powdered medication (blue cap).

Notice how the tPA is powder form.

In the box you will also find the package insert and a dual sided spike which is also sterile. The spike is the same on both sides, and has a dual channel so that air and fluid can flow in opposite directions.

Step 2

Under sterile conditions remove the cap of the saline vial. Holding the vial in the upright position, spike the vial.

Step 3

Continuing under sterile conditions, remove the cap from the powdered tPA vial. Hold the saline vial firmly in the upright position. With your other hand hold the tPA upside down, and lower the vial down onto the spike.

With both vials firmly spiked, invert both vials together. At this point, the saline will on top and will flow from the saline vial into the tPA vial. Hold the vials firmly, because the high center of gravity will make them unsteady. This process will take about 1 minute. Do not agitate the vials during this process.

Step 4

One all of the saline is in the tPA vial, grasp the flanges and decannulate the tPA vial by lifting up on the spike and saline vial.

Step 5

Gentle swirling will thoroughly mix the contents of the tPA vial. The medication is now ready. It can be drawn up and administered based on the indication and dosing regimen. Be sure to dispose your sharps.

29-year-old man with history of type 1 diabetes mellitus and currently living in a hotel, presented to the emergency department with 2-weeks of feeling ill with had accelerated and was much worse over the last 2 days. This included a productive cough, subject fevers, and frequent vomiting. He was brought in by his brother, and the patient was appeared ill, was somnolent, confused, and only oriented to self. his blood pressure was 78/43 mmHg, pulse 146 bpm, respiratory rate 26, 37.2deg C, SpO2 96%. An finger stick blood glucose measurement read HIGH. A cardiogram was also obtained.

This is a regular wide complex tachycardia. the first question you need to to determine in these cases is if the patient is stable or unstable. In this situation, the patient was hypotensive with altered mental status. He was electrically cardioverted using the synchronized setting and a voltage setting of 150 J. He was then immediately given 3 ampules of calcium gluconate and 3 ampules of sodium bicarbonate.

This is the correct treatment. The physicians inferred from the severe hyperglycemia that the patient may be hyperkalemic, which was the cause of the wide complex tachycardia. given that he was unstable electrical cardioversion was the first step, quickly followed by calcium to help stabilize the myocardium. The bicarbonate is given to facilitate the intracellular shift of potassium. The patient was additionally treatment with 2 L 0.9% saline bolus, 10 units SC insulin aspart were given.

Immediately after cardioversion the following cardiogram was obtained.

What is most impressive is the peaked T-waves consistent with hyperkalemia. His chemistry panel eventually returned which showed at presentation he had a glucose of 1120 mg/dl and a potassium of 6.6 mEq/L.

Androgue (Medicine 1986;65(3):163) created a formula to predict the potassium at admission in DKA.

K+ = 25.4 – (3.02 x pH) + (0.001 x glucose) + (0.028 x Anion Gap)

However in our case it under predicts the potassium, however the paper gives an excellent reviewing he mechanism of hyperkalemia in hyperglycemia.

Unfortunately the patient’s mental status did not improve significantly, and ultimately required orotracheal intubation and mechanical ventilation. He was admitted to the MICU where he continued on an insulin protocol overnight. About 10 hours after admission his anion gap had closed, and he was transitioned to long-acting insulin glargine. A repeat ECG at this time showed return of a normal sinus.

The patient ultimately did well and was discharged from the hospital.

Toxicology is a deep complex topic area, which can devour a disproportionate amount of studying time in preparation for the boards. Unlike many other subjects however, it lends itself to some word associations and other high value studyy. This list has been compiled to facilitate some rapid review.

Basic Word Associations

• Acetaminophen – NAC
• Anticholinergic Toxidrome (Jimsonweed, Benadryl, Atropine) – Physostigmine
• Benzodiazepine – Flumazenil
• Beta Blocker – Glucagon
• Calcium-Channel Blocker – Calcium, Insulin
• CO – High Flow O2, Hyperbaric Therapy
• Cholinergic Toxidrome – Atropine, Pralidoxime (2-PAM)
• Cyanide – Sodium Nitrite, Sodium Thiosulfate, Hydroxocobalamin
• Digoxin – Fab Fragments (Digibind/Digifab)
• Ethylene Glycol/Methanol – Ethanol, Fomepizole, Dialysis
• Methemoglobinemia (Benzocaine, Lidocaine – Methylene Blue
• INH – Pyridoxine (Vitamin B6)
• Heavy Metals – Chelation
• Opiates – Naloxone
• ASA – Sodium Bicarbonate Alkalinization
• Sulfonylureas (Glipizide/Glyburide) – Octreotide
• Valproic Acid – Carnitine
• TCAs – Sodium Bicarbonate
• Hydrofluoric Acid – Calcium

Pharmacologic Effects of TCAs

Toxic Alcohols

• Isopropanol –> Acetone = Ketosis w/o Acidosis
• Methanol –> Formic Acid –> Optic Nerve/Retina
• Ethylene Glycol –> Glycolic Acid –> Oxalic Acid –> Calcium Oxalate –> Kidney
• Anion Gap = Na+ – (Cl- + HCO3-)
  • ↑AG due to unmeasured anions  organic acid metabolites.
• Osmolar Gap = 2Na+ + (BUN/2.8) + (Glucose/18) + (EtOH/4.6)
  • ↑ OG due to unmeasured parent compound.
• HD Indications:
  • End-Organ Toxicity
  • Severe Acidosis – after resuscitation
  • Methanol > 50

Cyanide Treatments

• Hydroxocobalamin is new standard if available.
• Nitrites – Induce methemoglobinemia. Methgb + CN –> Cyanomethgb
• Thiosulfate – Thiosulfate + CN –> Thiocyanate
• Hydroxocobalamin – Hydroxocobalamin + CN –> Cyanocobalamin

Digoxin

• Inhibits function of Na+-K+-ATPase.
• Dosing:
  • Unknown Level w/Severe Toxicity: 10 vials for acute and 5 vials for chronic intoxication.
  • Known Amount Ingested: 2 vials per 5 mg ingested
  • Calculation: # DigiFab/Digibind Vials = (serum digoxin level (ng/mL) x body weight (kg))/100

Methemoglobinemia

• Inducers: Benzocaine, Lidocaine, Chloroquine, Dapsone, Pyridium, G-6-PD Deficiency
• MetHgb & Sat Monitoring: Falsely low reading of O2 sat -> 84% despite supplemental O2.
• % MetHgb and symptoms:
  • 3-15%: Slight discoloration of skin (pale/gray/blue) may be present.
  • 15-20%: Cyanosis present, but pt may be relatively asymptomatic.
  • 25-50%: HA, Lightheadedness, Syncope, Dyspnea, Chest Pain, Palpitations, Weakness, Confusion
  • 50-70%: Profound metabolic acidosis, AMS, Seizures, coma, dysrhythmias

Clinical Features

Two major categories: minor heat illness [heat edema, prickly heat, heat syncope, heat cramps, and heat exhaustion] and major syndromes [heat stroke].

Heat Cramps

• Involuntary, spasmodic contractions of skeletal muscles, usually of the calves, occasionally the thighs and shoulders.
• Self-limited, no significant morbidity, patient’s chief complaint will be pain.
• Due to relative deficiency of sodium, potassium, and fluid at a cellular level.
• Treat with fluids and salt replacement PO or IV.
• Complications: rarely rhabdomyolysis secondary to diffuse and protracted muscle spasm
• Prevented by maintaining adequate salt intake and drinking commercial electrolyte beverages.

Heat syncope

• Variant of postural hypotension resulting from the cumulative effect of relative volume depletion, peripheral vasodilatation, and decreased vasomotor tone.
• Occurs in nonacclimatized individuals during the early stages of heat exposure.
• Evaluation includes exclusion of metabolic, cardiovascular, and neurologic disorders that produce syncope.
• Treat with rest, removal from the heat source, PO or IV rehydration.

Heat Exhaustion

• Acute heat illness that reflects significant volume depletion and may or may not have an elevated core temperature.
• Symptoms: weakness, malaise, lightheadedness, fatigue, dizziness, nausea, vomiting, frontal headache, and myalgias.
• Clinical manifestations: orthostatic hypotension, sinus tachycardia, tachypnea, diaphoresis, and syncope, core temp can range from normal to 40°C.
• Mental status remains normal.
• Treat with volume, electrolyte replacement and rest.
• Complications: can progress to heat stroke.

Heat Stroke

• Core temperature higher than 40°C, CNS dysfunction, and anhidrosis.
• High mortality rate, multiple organ system involvement.
• CNS dysfunction can include: irritability, confusion, bizarre behavior, combativeness, hallucinations, seizures, or coma, ataxia.
• Neurologic abnormalities can include plantar responses, decorticate and decerebrate posturing, hemiplegia, seizure.
• Differential:
  • NMS.
  • Serotonin syndrome.
  • Infections: sepsis, meningitis, encephalitis, tetanus, typhoid.
  • Endocrine: DKA, thyroid storm.
  • Neuro: status epilepticus, hemorrhage.

Treatment

This patient suffered a cardiac arrest and was intubated in the field. He arrived in our stabilization room with ongonig BVM ventilation and LUCAS CPR. He was noted to have massive gastric distension.

As you can from the cross table radiograph, the distal tip of the King Airway has wedged itself in the pharynx and folded against itself. It is not seated properly against the hypopharynx. While this was providing ventilation, it also stented open the esophagus leading to a large amount of gastric insufflation.

Take a look at this really remarkable ultrasound image, not so much for it immediate clinical utility, but for its rarity.

A patient presented with numerous self-inflicted cuts all over the body including bilateral extremities, torso, and neck. Arrived profusely bleeding, and clearly needs to go to the operating theater.

Ultrasound of the right neck reveals the classic appearance of air within the internal jugular vein. This is evident by the hyper-echoic reflections with “dirty” distal shadowing. It is not hypo-echoic as is commonly assumed, because air has a lower ability to conduct sound than tissue or fluid hence it shows up brightly with a “reflective” quality.

They patient under went surgery and did well.

26-year-old woman cigarette smoker otherwise healthy. Presented with one week of neck swelling. Little pain. History of frequent pharyngitis with last episode about 1 week ago. Treated with course of azithromycin.

What is most striking is the left internal jugular clot and pronounced adenopathy. Note the cavitary apical lung mass on the left. A dedicated Chest CT showed numerous other nodules.

Microbiology demonstrated Fusobacterium necrophorum and was treated with a course of antibiotics. She did well with a complete recovery.

There is very little known about the difference between the various types of headaches. In the ED the primary concern is to separate primary from secondary causes of headache. Primary headaches are those that are not caused by a secondary medical condition, and are usually divided into migraine, tension, and cluster headaches.

Migraine headaches usually last 4-72 hours, are unilateral and pulsating in character. Almost always aggravated by routine activity, and can be associated with nausea or photophobia. The can sometimes be preceded by an aura or scotoma. Five separate attacks are required to receive a formal diagnosis.

The etiology of migraine headaches involve cortical spreading of depressed electrical activity. This leads to abnormal thalamic pain modulation. This cascade is activated by various factors and various levels related to a genetic predisposition.

Tension headaches are shorter duration lasting between 30 minutes to 7 days. Patients often describe them as pressure and bilateral, and in contrast to migraines they are not typically aggravated by activity.

If the patient’s symptoms don’t meet the diagnostic criteria listed above for one of the other category of headaches, they are usually classified as migrainous.

Secondary headaches are brought on by an underlying medical condition. The largest categories are meningitis, subarachnoid hemorrhage, vascular disease, toothache, and sinusitis. There is a long list of etiologies (See excellent DDx on Life in the Fast Lane).

The diagnosis of a primary headache is made by ruling out an organic disorder through the history, physical, or findings. It can also be suggested when an organic disorder was suggested and then ruled out. It is important to note that sometimes an organic disorder is present but the headache is not related to it.

Many secondary headaches are actually migraine headaches triggered by a malignant stimulus.

There is a spectrum of headaches upon which all primary headaches lie, the effectiveness of the medication is not related to its defined nature. Treatment options can include triptans, dopamine antagonists, NSAIDs, sleep. For those with recurrent headaches prophylactic medications can be used such as depakote or dexamethasone. An important principal is to never use opiods for primary headache. It is not supported by any guideline.

We have previous posted a detailed discussion of headache treatment options in the emergency department (link).

In the ED the primary concern is to separate primary from secondary causes of headache. Primary headaches are those that are not caused by a secondary medical condition.

Primary headaches

• Tension headache
• Migraine
• Cluster headache.

Secondary headaches

Intracranial

• Cerebral space-occupying lesion (cerebral aneurysm, AVM, tumour, haematoma)
• Infection (abscess, meningitis, encephalitis)
• Haemorrhage (intracerebral, subarachnoid, subdural)
• Cerebral venous thrombosis
• Post-traumatic (subdural, extradural, cerebral contusion)
• Benign intracranial hypertension
• Cerebral vasculitis such as SLE
• Post-lumbar puncture (worse on standing)
• Posterior reversible encephalopathy syndrome (a syndrome of headaches, altered mental status, seizures, and visual loss associated with white matter vasogenic edema predominantly affecting the posterior occipital and parietal lobes of the brain; usually occurring in patients who are hypertensive or receiving immunosuppressant’s).

Local

• Musculo-skeletal: TMJ dysfunction
• Vascular: Temporal arteritis
• Neuralgia (greater occipital, glossopharyngeal, trigeminal)
• SUNCT (Shortlasting Unilateral Neuralgiform Headache attacks with Conjunctival injection and Tearing) syndrome
• Eyes: Glaucoma (always examine for a painful red eye with cloudy cornea, and ovoid fixed pupil)
• Ears/Sinus: Sinusitis, otitis media, mastoiditis
• Neck: Cervical osteoarthritis, cervicogenic headache
• Teeth: Dental caries, tooth abscess

Systemic

• Malignant hypertension
• Hypercapnia
• Carbon monoxide poisoning
• Systemic infection
• Viral infection (Dengue fever, Ross River)
• Pre-eclampsia (Is the patient pregnant?)
• Drug related
• Nitrates, Calcium-channel blockers, NSAIDs
• Medication overuse headache

HCMC has created a rapid sequence intubation (RSI) checklist, and printed it in large poster format. It is hung above our airway cart in the stabilization bay.

This is organized around the ‘P’s. There are more detailed considerations under each heading to the right as well. This checklist is designed to be a quick visual reference during RSI to remind you to plan, position, pre-oxygenate (and provide apneic oxygenation with nasal cannula), and be deliberate with your preparation and decision-making.

Most importantly, it includes post-intubation steps, that can often be overlooked as the team moves on to other resuscitation steps after securing the airway.

You are sitting watching re-runs of ‘Jeopardy’ and having a beer when breaking news shows a building collapse that has occurred several blocks from your home. Though you think you know the answer to the puzzle, you are torn between solving it before the contestant does and rushing to the scene. What should you do?

• Solve the puzzle–for one thing, unless you know yourself to be the only provider with the skill set necessary you should not respond to ANY incident after having any alcohol–even if everything goes well, questions will still be asked.
• Hospital personnel in the field seldom is a good situation–unless you are used to working in that environment you don’t have the protective equipment and scene awareness that you need, and you are not able to medically do what you usually would do so you’re ‘off your game’ and likely to make mistakes–unfamiliar resources, limited capabilities. In Singapore, the airport disaster plan called for ED personnel to be transported to the scene to assist–which was done when a plane crashed on take-off during a typhoon. The ED providers arrived after most of the casualties were already gone, got soaked in their scrubs, many developed hypothermia, and basically contributed negatively to the response as a further drain on organizational resources. An ER nurse who rushed to the Oklahoma City bombing scene to assist was killed by falling debris. And the list goes on. It’s also very difficult to integrate into the response effectively unless you are well known to the EMS providers. So basically, unless you have a response role at the scene, don’t bother going to the site.

After going to the grocery store for more Ho-Ho’s and frozen pizza, you are driving home and witness a building collapse. What should you do?

• If you happen to be ON the scene of a mass casualty event right after it happens, you can be of significant help in the early minutes to responding EMS personnel IF you can keep yourself safe.
• Scene safety is critical–park somewhere safe and out of the way of responding public safety. Look all around you BEFORE you commit to helping–including above you… watch out for sharp debris, live power sources, leaking natural gas, further structural collapse potential, hazardous materials (if there’s any natural gas odor or other hazmat risk–chlorine leak or whatever just GET OUT and take as many ambulatory patients as you can with you to a location at least a few blocks away (and upwind, for leaking chemicals).
• Your primary goal is to start triaging–direct ambulatory patients to a single spot that is safe and recognizable ‘go to the parking lot over there’ and identify the non-ambulatory. Determine which have altered mental status, difficulty breathing, or signs of severe hemorrhage or shock (all ‘red’ criteria)–there’s not a lot of treatment you can do (unless your vehicle is equipped with a spare stab room), but you can be a huge help sorting patients for transport prior to and even after EMS arrival and helping with basic treatments as supplies become available (controlling bleeding, basic splinting, etc.)
• Be very careful of trying to help ‘rescue’ anybody–unless you are VERY comfortable that there’s no structural issues or electrical lines and no falling debris this can be inherently dangerous–if you have to do something because of an immediate safety threat to the patient don’t worry about spinal precautions, just get the patient away from danger generally by dragging them under the shoulders while supporting the head to maintain what neutral alignment of the c-spine that you can
• As soon as EMS arrives, hook up with the initial crew and/or a supervisor and identify yourself and your skills – do what they ask you to. If you’re in a different area (not your local EMS system), identify yourself to an EMS provider and ask who the EMS supervisor / EMS command is, then hook up with them and see if you can assist. If you are an MD it’s particularly helpful in our area to let the EMS supervisor know you have a radio number (if you do)–that establishes a lot more credibility and that you may be somewhat useful, as well as can provide orders directly if required
• Once EMS resources are adequate, if a disaster alert is declared at your hospital consider reporting there. Usually by this time though, unless the incident is truly massive we already have more help than we need at the hospital.

On your way home, you come across a car accident – two persons are injured. What should you do?

• If you have medical training and arrive at an accident you are generally expected to assist to the level of your ability and state ‘Good Samaritan’ laws protect you from liability Except for willful and wanton misconduct–which may apply to some aspects of your Friday night, but not to your medical care.
• If required, use your vehicle to block traffic so that you can safely help (position your car with hazard flashers on a reasonable distance behind the accident and block the traffic lane–if there’s more than one lane straddle the one that the accident is in and the one adjacent so that cars are not passing inches from the vehicles and victims involved (but be ready to move it as soon as police arrive if asked)–don’t park too close–if your car gets hit you don’t want it getting pushed into the already involved cars and patients)–get somebody to direct traffic around the accident if needed.
• Your primary hazard is getting hit by another car that is looking at the accident and not at you or plows into the involved vehicles (due to icy conditions, texting, or whatever). There is also the ‘moth effect’ phenomenon where drivers steer towards the flashing lights of police and other vehicles and wind up hitting them (you tend to drift unconsciously toward what you are looking at – true for bike riding, car driving, etc.).
• Make sure first that you don’t have any power lines down.
• Assure that the engines/ignitions are turned off (particularly an issue with hybrids to assure the battery is off).
• Look quickly for airbags that did not deploy–(i.e. one front airbag didn’t go off) these can deploy unexpectedly, as well as for leaking fuel (which is common). Draw this to the attention of fire when they arrive and make sure there’s no ignition sources around. We have seen people lighting up at the scene of a leaking fuel tanker truck.
• If you have to get access–try the doors–often you can find one that will open and then 1-2 people can usually bend the door open. If you have to break glass, strike the lower corner of the window panel with a sharp object. It should all crumble and fall out in a dramatic and satisfying manner Except for the windshield–do NOT try to go after the windshield–a waste of time.
• Identify yourself to the patients and identify injuries and any entrapment that the victims have. Maintain airways, control bleeding, and keep spinal alignment as required until help arrives. If the victims are uninjured and can get out of the vehicle it may be best to get them up on the sidewalk or another area of safety. Once EMS arrives tell them what you have done so far and then generally get out of the way and let them take over–we often find that medical providers are resistant to this transition–but EMS does this every day, and we don’t, so don’t feel like you’re abandoning the patient by letting EMS take over (in more rare cases, if you have advanced skills and are in an area served by basic life support ambulances, you may have to continue to be involved and provide ongoing medical support to the degree that you can with the equipment you have available).

Enjoy your Ho-Ho’s and pizza. The correct question for the answer is “What is Uruguay?”.

By Dr. John Hick, Medical Director for the Office of Emergency Preparedness with the Minnesota Department of Health.

I practice at Hennepin County Medical Center, a large inner city academic Level 1 Trauma Center. Like all such facilities we have been under a tremendous pressure to reduce costs, and pharmaceutical costs have been a large target. To make us physicians more aware of our prescribing patterns, the Pharmacy has provided us two fascinating lists.

The first list is the top 30 drugs ordered in the emergency department during 2012. It is not very surprising that 6 of the top 10 medications are pain relievers. Interestingly, droperidol (often combined in the same syringe with diphenhydramine) was our #4 used medication, often being given for headache, nausea/vomiting, and agitation. Of note, quetiapine is primarily ordered by psychiatric emergency physicians and is not a typical ED medication.

The second list however, shows the top 30 medications by cost. To protect confidential pricing information, I have normalized the data to $100. Alteplase tops the list and is used almost exclusively for stroke and pulmonary embolism. Surprising to me was tetanus-diptheria-acellular pertussis which is given nonchalantly for our trauma patients. Our first line pain medication is liquid oxycodone (to prevent cheeking), and no surprise it comes in #3. Droperidol, despite being generic is given in large quantities making its total bill high enough to place it #4 on the list. Olanzapine which is only #24 on the frequency list, has been alternative for us when droperidol has been on shortage, and given is patent status, has cost our hospital just about as much as droperidol despite being used 1/2 less frequently.

Cost estimates are based on drug purchase cost only. For pharmacy-prepared medications, this does not include cost of labor or supplies. Includes medications dispensed by omnicell machines, ED floor stock items and items commonly sent to ED from pharmacy. For compounded items, cost was only based on active drug ingredient.

As droperidol goes back on shortage, I wanted to give a brief review of primary headache treatments. Most therapies for primary headaches have a ~60% rate of pain relief, and there is no predictable overlap between drug classes, so if one class doesn’t work, try another class of medications.

1. Triptans:  The constellation of symptoms and their duration do not appear related to the effectiveness of these medications for any primary headache, so use them on any of them in patients who aren’t pregnant and don’t have cardiac risk factors putting them at risk from its transient vaso-spastic effects
   1. Ellitriptan (Relpax) 40 mg po, this should be your first line in the ED, multiple studies have shown it to be as effective as sub cutaneous sumatriptan and better than the other oral ones.
   2. Sumatriptan 6mg sub cu, no more effective than Relpax but comes in a shot. Don’t use the oral version.
2. Dopamine Antagonists
   1. Droperidol: 2.5 mg IV and 5 mg IM have been shown to be superior to other drugs in the is class, the principle side effect is sedation, which is far more common than akithesia when we have studied it here, so keep that in mind when deciding whether to pre-treat with Benadryl.
   2. Olanzapine 10 mg IM: Found it to be similar to droperidol in a 2008 study.
   3. Compazine 10 mg IM/IV less effective than droperidol similar to reglan for effectiveness and side effects.
   4. Reglan 10 mg IV less effective than droperidol same as Compazine for side effects.
3. Sleep Inducing Agents
   1. Secobarbital: has great data for relieving headaches but its not on our formulary, send patients home with a dose, they take it in bed and wake up without a headache.  I’ve tried this with headache who failed triptans and don’t want droperidol using ambien 10 mg with some success.
   2. Benzos: the shorter acting the better, inducing sleep is the goal.

Compiled by Dr. James Miner, Associate Professor, Department of Emergency Medicine, Hennepin County Medical Center.

There is a historic collapse at the sports complex three blocks from your facility (structural, this time, not the on the field). Hundreds of people are rushing to your hospital for care.

What can you say generally about the first arriving victims and what can you do about them?

• Usually most of the initial victims will be the least injured – they were more mobile and able to get out of the building
• Keep walking patients out of the ED until you know that you have room and resources to treat them – put them at triage and in the lobby areas and get personnel out there to screen them
• Keep them busy – have them fill out the top paper section of their patient encounter (clipboards and forms are in the triage bins) or have them assist other patients – provide support, etc.

What is the main risk to the more severely injured patients?

• The higher the number of patients that are not severely injured (or tagged as ‘red’ or critical that are actually not) the worse the outcome for the critically injured (as resources are not available to them – this isn’t usually an overt thing, but lots of little distractions and issues that add up to sub-optimal outcomes) – this is known as ‘over-triage’ – in NYC on 9-11 the overtriage rates (not severe to severe casualties) were as high as 95%, and the mortality rate of the severely injured was 44% at that hospital vs. goal of 10% – there is a nearly linear correlation between the ratio of less-injured casualties : seriously injured and the mortality for these patients over many incidents in many countries

What are the key bottlenecks in triage?

• Front door/ambulance entrance – who waits, who gets a a bed, who’s critical
• US – everyone’s going to want them, but there’s only a few machines – make sure you get your FAST done FAST and make the machine available – consider making FAST part of the ambulance door triage for non-ambulatory patients
• CT – who needs one? And how can you avoid the ‘pan-scan’ and concentrate on heads and things that you MUST know right now
• OR – who needs it now (vs. who can wait – ortho and limb-related stuff can wait, most truncal and vascular cannot)

If things get really overwhelming, what are the priorities?

• Concentrate on the interventions that make the biggest difference with the least time and materials
• Control external hemorrhage (pack the wounds with gauze and use ACE wraps – works well, tourniquet if this doesn’t work)
• Decompress tension pneumothorax
• Manage airway obstructions
• If you have the option for OR send only those with shock, positive FAST and isolated abdominal injuries

What factors should you consider if you cannot take care of all the severely injured?

• Prognosis / odds of survival
• Resources required to treat them fully
• Underlying disease if it has an extremely poor short-term prognosis (cirrhosis, for example) – this is very limited
• Age is NOT a good triage indicator aside from older than 85 years (very few patients) and should not generally be used aside from advanced age in multi-system trauma or severe burns
• DON’T forget that even if you aren’t able to provide usual care (say you triage an 90% burn victim to expectant management) that you still have to provide symptom control / palliative care including analgesia, anti-emetics, anxiety control, etc. So just because you can’t do what you normally do doesn’t mean the patient doesn’t get care…

You find somebody to take over the Triage role and are assigned to three patients in the ED now what?

• Use your clinical skill – stop bleeding, splint fractures, etc.
• Don’t do definitive procedures until we know we can take the time to do it – (usually most of the victims arrive within the first 90 minutes after a mass casualty incident)
• Use US liberally for triage
• Only Xrays you should probably be ordering are chest and pelvis
• Work with your Team Center Leader to help prioritize access for procedures, CT, admission, OR, etc.

Congrats, your shift is now over – good luck facing the national media on the way out of the hospital!

Compiled by Dr. John Hick, Medical Director for the Office of Emergency Preparedness with the Minnesota Department of Health.

Nasotracheal intubation is an essential skill that allows a flexible approach to airway management. In order for nasotracheal intubation to be successful it requires patient respiratory effort and air exchange. The Beck Airway Airflow Monitor (BAAM) is a device which when attached to a 15 mm endotracheal tube adapter, magnifies airway-airflow sounds, producing a whistling sound which greatly aids in correct endotracheal tube placement.

Instructions

1. Attach the orange BAAM® device to the 15 mm adaptor of the appropriate sized endotracheal tube, the device will attach only one-way to the tube.
2. Pre-oxygenate and/or ventilate while preparing the patient for nasotracheal intubation.
3. Perform nasotracheal intubation. As the ET Tube nears the larynx an audible increase in whistling will be heard from the device, indicating that the tip of the endotracheal tube is near the entrance to the trachea.
4. Carefully advance the endotracheal tube through larynx into the trachea when device and airway sounds are at their peak. Confirm that successful intubation has occurred.
5. Once intubated, quickly remove the BAAM® device and begin ventilating the patient.
6. Confirm tube placement by visualization, auscultation, and/or capnography.

Precautions

• An unobstructed endotracheal tube with its tip located in the pharynx can also produce the whistle sound, therefore, it is important to always confirm placement in the trachea.
• Due to the narrow aperture of the BAAM device, it is never to be left attached to the endotracheal tube for greater the 15 seconds at any time for assessment of the previously intubated patient. Partial airway obstruction, hypoxia and increased airway pressure can occur if left in place for prolonged periods of time.

Indications

• As an adjunct to blind nasotracheal intubation in the patient with spontaneous respirations.
• As aid to re-confirming airway patency or re-assessing respiratory effort in the intubated patient with respiratory effort. This device is not to be used as the primary method for assessing airway patency in the intubated patient.

Contraindications

• Apnea, or inability to hear device during endotracheal tube insertion.

References

1. Cook RT Jr, Stene JK Jr.. The BAAM and endotrol endotracheal tube for blind oral intubation. Clin Anesth. 1993 Sep-Oct;5(5):431.

Incessant ventricular fibrillation is difficult to manage. The mainstays of treatment include:

• LUCAS CPR and ResQPod impedance threshold device
• Multiple defibrillations
• Amiodarone
• Magnesium
• Lidocaine
• Esmolol

We have previously explored the option of using high energy defibrillations for this situation.

A novel technique which has been discussed in the literature is the stellate ganglion block. The stellate ganglion is part of the sympathetic chain formed by the inferior cervical and first thoracic ganglia, and provides sympathetic innervation to the upper extremities, head, neck, and heart. The procedure can be performed blindly, but usually done under fluoroscopy for reflex sympathetic dystrophy by pain specialists. Direct ultrasound guidance may allow this procedure to be performed with accuracy during resuscitation efforts. By blocking the sympathetic output, to the heart there is the possibility of ceasing the ventricular storm. There is a risk however of residual left ventricular dysfunction.

Further studies on this are underway.

Detailed instructions of the procedure.

Equipment

• CHG prep.
• 1% buffered lido with 27 ga 1.5 in needle.
• 25 ga 3.5 in spinal needle.
• 7 cc 1% lidocaine with epinephrine or 0.25% bupivicaine.
• Ultrasound with high-frequency linear probe.

Procedure

1. Place  patient in supine position with neck extended.
2. Palpate to identify the thyroid cartilage and cricoid cartilage. Place a finger in groove lateral to trachea and palpate a bony prominence known as Chassaigniac tubercle. This is the C6 level and should be marked.
3. With ultrasound, start in the transverse orientation at the C6 level. Visualize the trachea and cricoid cartilage. Move the probe slightly laterally. Visualize the Chassaigniac tubercle, thyroid.
4. Move the probe slightly inferior, until the bony process flattens out.
5. Using color Doppler indentify the perforating thyroid arteries, carotid artiery, and verterbal artery.
6. Anesthestize the site with lidocaine.
7. Advance a 2.5 ga 3.5 in needle through the tract to contact the os at C7. The needle is backed off slightly. Verify no blood return on aspiration to confirm that you are not in a vascular space.
8. Inject 6-7 ml of anesthetic.

References

1. Circulation 2000;102:742. Treating Electrical Storm–Sympathetic Blockade vs ACLS Guided-Therapy.
2. PainMedicine 2011;12:1196. Left Stellate Ganglion Blockade for the Management of Drug-Resistant Electrical Storm.
3. TexHeartInstJ 2011;38:409. Left Stellate Ganglion Block for Continuous Ventricular Arrhythmias.
4. AnesthAnalg 1994;79:1082. Left Stellate Ganglion Block Impairs Left Ventricular Function.

My preferred method is the anterior-medial approach. Place the patient in the supine position with knee flexed, and foot plantar flexed and resting flat on the bed. An high-frequency linear probe is most useful for identifying the detailed structures. Using a combination of palpation and ultrasound, identify the anatomical landmarks including the Extensor digitorum, tibialis anterior, Extensor hallicus longus, and the doralis pedis artery (which is deep and lateral to to the extensor hallicus longus).

The effusion appears as an hypoechoic structure just distal to the tibia in the tibiotalar recess. The probe should be medial to the tibialis anterior tendon. The procedure should be performed in sterile conditions.

The fluid should be sent for cell count and differential, culture, and crystal analysis. An interesting method of distinguishing septic arthritis, from underlying gouty arthritis may be the measurement of lactate (S

• ynovial Lactic Acid and Septic Arthritis. JAMA. 2007;298(1):37).

Zones of the Neck

• Defined by mandible, cricoid cartilage, and sternal notch.
• Most injuries sustained in Zone II, especially carotid injuries
• Zone I mortality high due to intrathoracic injuries.
• Posterior triangle with few vital structures. Important exception is subclavian at risk just above clavicle.

 Rapid Assessment

• Speak (voice change: hoarse, dysphonia)
• Cough (hemoptysis)
• Swallow (dysphagia)
• Carotid auscultation (bruit, thrill)
• Symmetric pulses

Penetrating Trauma

• Based on the Eastern Association for the Surgery of Trauma (EAST) Guidelines
• Unstable: Surgical exploration
• Stable: CTA initial study of choice all zones and blunt
• C-spine immobilization not required for isolated penetrating trauma if patient awake and neuro intact1.

1. Arterial injury

• CTA or US in Zone II
• US up to 100% Sn & Sp for arterial injury
• Angio if positive or inconclusive (s.a. streak artifact)
•  IR can diagnose and embolize (esp Zone III)
• Noncontrast CT sufficient if trajectory remote to vessels

2. Laryngeal injuries

• – Direct laryngoscopy for suspicious wounds
• – CTA

3. Esophageal injuries

• Not excluded by normal x-rays
• Contrast esophagoscopy or esophagraphy (Gastrografin → Barium → Endoscopy)
• Typically done after resuscitative phase

Blunt Neck Trauma

1. Cerebrovascular injuries

• Any neurologic abnormality not attributable to other injuries
• Suspected arterial epistaxis
• High risk head trauma
• US not adequate, CTA is study of choice

2. Esophageal injuries

• Very rare and evaluation only required for symptoms

Cardiac pacemakers and their malfunctions are often daunting for the emergency physician to diagnose and manage. This is the first part of a series covering this area.

• Part 1. Pitfalls and pearls of temporary transvenous pacing.
• Part 2. Procedural instructions for placing a transvenous pacemaker and the use of the temporary pacer generator.
• Part 3. Introduction to permanent pacemakers and ICDs.
• Part 4. Diagnosing problems permanent pacemakers and ICDs.

On to a case for discussion.

A nursing patient was brought to the emergency department for evaluation of lethargy, “being floppy”, and hypotension (90/50 mmHg). He was known to have right-sided systolic dysfunction, medication controlled hypertension, insulin-controlled type 2 diabetes mellitus, and CKD Stage III.

On physical exam he was noted to be obtunded and bradycardic. IV access was established, and initial laboratory tests were sent. He was orotracheally intubated without difficulty and easily ventilated. Atropine was given without an increase in his heart rate. He was placed on transcutaneous pacing. We presumed the patient was suffering from hyperkalemia and he was given calcium gluconate, and shifted with insulin/glucose. It was difficult to establish good capture. Multiple different pad locations were attempted, and eventually we were able to get intermittent capture using a right-parasternal and apex pad location.

A 12-lead ECG was obtained as shown below. This was interpreted as sinus bradycardia, with a narrow QRS complex and significant T-waves abnormalities. There did not appear to be any ST-segment or T-wave changes concerning for ischemia. The large voltages recorded on the right-side of the strip occurred when the transcutaneous pacer was restarted.

A bedside cardiac ultrasound confirmed bradycardia. Contractility was adequate and there were no gross focal wall motion abnormalities.

The remainder of the FAST exam was was notable for free fluid in the abdomen. This included fluid in Morrison’s pouch, suprapubic region, splenorenal angle, as well as bilateral pleural effusions. This was presumed to be ascites. Evaluation of his IVC while being positively pressure ventilated showed a dilated vessel without significant respiratory variation. Images from the FAST exam and a video clip of the IVC ultrasound are shown below.

At this point, we got back initial laboratory tests. His blood counts were normal. Chemistry panel revealed a potassium of 7.4 mEq/dl. He was given additional calcium gluconate. Given that the transcutaneous pacing was intermittent, we decided to place a transvenous pacing wire (details of this procedure in Part 2). Below you can visualize the floating balloon in the right ventricle. It is visible as the hyperechoic structure with shadowing that is seen in the right ventricle.

Unfortunately, a chest radiograph and ECG were not immediately obtained in the ED. The patient was admitted to the Medicine ICU, and shortly thereafter was noticed to have only intermittent capture. A supine chest radiograph was obtained, which is shown below.

This is a fairly difficulty radiograph to interpret. The pacer pads can be seen over the left hemithorax. The pacer can be seen in the internal jugular vein and descending the SVC to the heart. It is looped in the right ventricle, and there is likely part of the wire that crosses the tricuspid valve. Below is a schematic of the pacer wire to help you interpret the chest radiograph and visualize how the pacer wire was coiled.

The patient was turned for cares, and it was noticed that the morphology of rhythm recorded on cardiac telemetry had changed. A 12-lead ECG while being paced was obtained, and is shown below. As you can see there are pacer spikes prior to each p wave, and there is a narrow QRS complex. The axis of the p wave is inferior and to the left. This is means that the the pacer is atrial pacing, and likely at a location high up the ventricle. It is likely that the pacing tip had been pushed out of the ventricle and was not in contact with the right atrium wall. This was attributed to excessive slack in pacer wire because of the coiling, and a partially inflated floating balloon.

The patient was taken to the cardiac catheterization lab for repositioning of the pacing wire under fluoroscopy. The wire was confirmed to be coiled and almost tied in a knot. The tip was in the atria, and the floating balloon was partially inflated. It was respositioned without difficulty and excellent capture. The patient was returned to the MICU, and ultimately underwent emergent dialysis to correct the underlying hyperkalemia.

Procedures performed in the emergency department are performed on unstable patients under time-critical conditions can have many steps that introduce complications. Familiarity and checklists, can dramatically increase not only their success but also safety.

Cardiac pacing is can be a life-saving procedure. But there are many important lessons. Below are some of the most critical

• Before considering either transcutaneous or transvenous pacing for bradycardia, the patient should be evaluated for significant hypotension and other signs of hypoperfusion. If these are not present, the bradycardia can be observed.
• The floating balloon should be fully deflated.
• Remember that bradycardia is not always a primary cardiac issue such as sick sinus syndrome, atrioventricular block, or myocardial ischemia. Always consider secondary causes such as hyperkalemia, hypothyroidism, hypothermia, or overdose with beta-blockers, calcium channel blockers, digitalis, clonidine, or other antiarrhythmics.
• The right internal jugular vein is optimal for placing the transvenous pacer.
• Typically the pacer wire should be placed to a depth of about 40-45 cm if entering from the right internal jugular vein. It should be pre-measured on the patient before insertion.
• The manufacturer instructions and standard practice by the electrophysiologists are to use air in the floating balloon. There are case reports of the balloon rupture causing air embolism, most kits come with an inflation syringe that limit the amount of air to 0.75-1.0 cc. The use of saline can interfere with balloon deflation, and at least anecdotally makes it harder to float into place.
• The balloon should be fully deflated once properly positioned and achieving good capture.
• As you are placing the pacer wire, the patient should be monitored on continuous cardiac monitoring. Successful cardiac pacing with a properly placed pacing wire should demonstrate ventricular pacing with a LBBB morphology.
• An ECG and chest radiograph should be obtained immediately after placing the transvenous pacer wire and obtaining capture.
• The chest radiograph should be inspected for the path of the pacer wire. There should be no lops or coiling, and the pacer tip should seated in the apex of the right ventricle.
• The initial amperage should be set to 25 mA. Once capture has been achieved, this should reduced until you loose capture, and then doubled. Typically this is around 5 mA.
• The rate should be set at an adequately level to avoid hypotension, usually around 60 bpm.
• If the patient is poorly tolerating transcutaneous pacing, an alternative to transvenous pacing would be to intubate and sedate the patient.
• After any cardiac pacing whether transcutaneous or transvenous, when the pacing is removed there is a significant risk of asystole.

Tuberculosis is an endemic problem through most of the world. However, when it presents as active pulmonary disease in the United States, especially in nonimmigrrant, it is usually early in the disease process. This patient a native resident, had delayed seeking care for months.

The chest radiograph shows massive cavitary lesions, and sputum samples had an overwhelming AFB organism load. The following series of cuts from the CT chest that demonstrates the cavitation predominantly in the upper lobes.

On CT head imaging there was also evidence of tuberculomas.

We discussed in a previous post our algorithm for evaluation of clinically apparent globe injuries. However, this is less frequent than evaluating a patient with no clinically obvious globe injury.

Globe rupture is more often occult on presentation. The most frequent sites of rupture are not easily visualized, and more superficial injuries may block examination of the posterior segment. Very small sharp foreign bodies can enter the eye through small wounds that are difficult to visualize.

Our institution has developed the following protocol for evaluation of Clinically Non-Apparent Ruptured Globe Injuries and Severely Swollen Peri-Orbital Region and Inability to Easily Open Eye/Eyes

• Ultrasound of involved orbit using sterile ultrasound gel and high frequency US probe.
• Minimize applied pressure to orbit when performing ultrasound.
• Carefully remove all US gel from involved orbit. Use absolute minimal pressure to involved eye while removing US gel.
• Obtain CT scan of orbits or head if clinical suspicion is high for ocular injury or potential for intracranial injury.
• Call Ophthalmology if concerned for abnormal orbital ultrasound.

This is an incidental finding seen during routine contrast CT scans. In this case the patient was undergoing imaging as part of a trauma evaluation. There can be as much as 20-30 cc of air inadvertently injected. This can also occur during IV placement if poor technique is used.

The air typically collects in the right ventricle or proximal aorta, and is usually harmless.

Fracture of the base of the first metacarpal bone which extends into the carpometacarpal joint.[1] This intra-articular fracture is the most common type of fracture of the thumb. Caused by an axial force directed against the partially flexed metacarpal, such as during a fight or fall onto the thumb. In the ED they should be placed in a thumb spica splint, and referred for closed reduction and percutaneous pinning.

Demonstration of typical Takotsubo pattern of left ventricular dysfunction is well known. Several variants have recently been published, with one of the rarest being the reverse type of this syndrome, with hyperdynamic apex and complete akinesia of the base (as opposed to the classic apical ballooning)

The leads V4-V6 are removed and substituted for V7-V9 as shown below. On most EKg machines, the labels areno automatically changed so it is important to cross out the labels for V4-V6 and write in V7-V9. It is also helpful for future clinicians, if you note in your read that it is a posterior ECG.

A 45-year-old man with severe coronary heart disease s/p CABG but with an unprotected left main, presented to the emergency department for evaluation and suffered a ventricular fibrillation cardiac arrest. CPR and BVM ventilation was initiated immediately. The patient underwent an aggressive resuscitation effort with:

• LUCAS CPR and ResQPod impedance threshold device
• Multiple defibrillations
• Amiodarone
• Magnesium
• Lidocaine
• Esmolol

At this point the patient had received high-quality uninterrupted CPR, electrical defibrillations, inovasopressors, and antiarrhythmics. Despite this, the patient had persistent ventricular fibrillation. Intermittent cardiac ultrasound showed no cardiac activity. What options remain?

We decided to attempt high energy defibrillation. The use of a second defibrillator with separate pairs of electrodes allows 400 J of biphasic energy to be applied to depolarize a critical amount of myocardium. First described by Hoch, he found that patients who developed refractory ventricular fibrillation during electrophysiology procedures had restoration of regular rhythm.

High energy defibrillation is performed by attaching a second set of pads attached to a second defibrillator, ensuring that a second vector is established through the heart. At the time of defibrillation, both shock buttons are depressed as near-simultaneously as possible.

With all of these above efforts including the high energy defibrillation, the patient had brief ROSC, at which point he was taken to the cardiac catheterization lab. However, en route, he became bradycardic again, and LUCAS CPR had to be restarted. Angiography was performed with ongoing CPR, which showed a complete left main thrombosis. A thrombectory was performed and TIMI III flow was restored. We considered initiating extracorporeal membrane oxygenation, however, it was apparent that despite restoration of coronary flow, the patienthad no sustaining rhythm. He had pulseless electrical activity, that was not perfusing.

References:

1. Hoch et al. “Double sequential external shocks for refractory ventricular fibrillation.”  Journal of the American College of Cardiology. April 1994. 23(5): 1141.

This gentlemen presented with 3 hours of severe upper sternal chest pressure that radiated to his throat which he described as “strangulating”.

The initial ECG was concerning concerning for ST depression in the precordial leads that may be consistent with posterior stunning.

He was eventually brought emergently to the Cardiac Catheterization Lab and he was found to have 99% stenosis in the proximal segment of the 1st OM that gives rise to a good sized lateral branch. He was also found to have a 90% ulcerated plaque in the proximal RCA. Given the symptoms of chest pain and the sizeable wall motion abnormality on the echo in comparison to the size of his circumflex and his RCA, I decided that this could represent a co-culprit and I fixed both lesions. The left circumflex 1st OM lesion was fixed using thrombectomy and a 3.5 x 20 mm Promus Element DES post dilated a 3.5 x 15 NC balloon.

Evaluation of pediatric head trauma, especially the decision to obtain advanced imaging has significant risk/benefit trade-offs. Three major studies have been performed to aid the emergency physician and parents in this decision.

CATCH

• Canadian Assessment of Tomography for Childhood Head Injury
• CATCH: a clinical decision rule for the use of computed tomography in children with minor head injury. Osmond et. al. CMAJ. 182(4) 341-348, 2010
• Objective: Prospectively Derive an accurate and reliable clinical decision rule for the use of CT for children with minor head injury
• Enrolled 3866 pts from 10 Canadian hospitals with 7% being less than 2 years of age
• Inclusions
  • < 16 yo
  • Presenting within 24 hrs
  • Blunt trauma resulting in LOC, amnesia, witnessed disorientation, persistent vomiting (2 episodes 15 minutes apart) or persistent irritability (under 2 yo)
  • Initial GCS of at least 13
• Exclusion
  • Penetrating trauma, depressed skull fx, focal deficits, development delay or suspected abuse
• Methods
  • ED providers evaluated pts for 26 standardized clinical findings from history, general exam and neurological status.
  • Potential predictor variables were selected prior to initiation of trial via literature and pilot study
  • Recursion partitioning was used to combine variables to find best combination of predictor variables that were highly sensitive for detecting the outcome measure.
  • All those d/c without CT had 14 day telephone f/u.
  • Primary outcome: Was need for NSG intervention
  • Secondary outcome: Evidence of brain injury on CT.
• Results
  • Having any 4 of the high-risk factors predicting outcome of NSG intervention had a sensitivity of 100%
  • The presence of any of the 4 high-risk factors or 3 medium-risk factors in the rule would identify any CT-visible brain injury with a sensitivity of 98.1% (3 missed cases) (NPV 99.8)
  • 3 missed cases not identified by decision rule were an occipital skull fracture with small pneumocephalus, mild brain edema and small EDH. None required treatment

CHALICE

• Children’s Head Injury Algorithm for the Prediction of Important Clinical Events * Derivation of the children’s head injury algorithm for the prediction of important clinical events decision rule for head injury in children. Dunning et. al. Arch Dis Child 91, 885-891, 2006.
• Objective: Derive a sensitive clinical decision rule for the management of children with an acute head injury, which would identify children at high risk so as to undergo CT and allow remaining patients to be d/c.
• Enrolled 22, 772 pts from 10 hospitals in England
• Inclusions
  • Any pt with history or sign of injury to the head
• Exclusion
  • Refusal to consent
• Methods
  • ED providers evaluated pts for 40 standardized variable including mechanism of injury, signs and symptoms.
  • Potential predictor variables were selected prior to initiation of trial via literature and pilot study
  • Recursion partitioning was used to combine variables to find best combination of predictor variables that were highly sensitive for detecting the outcome measure.
  • Primary outcome: Was composite comprising death from head injury, NSG intervention or abnormality noted on head CT.
  • Secondary outcome: Presence of a skull fracture or admission to hospital.
• Results
  • Overall sensitivity of 98%. (NPV 99.9%)
  • Missed 4 patients.
  • 2 had depressed skull fractures missed on examination of 1st physician (Assume treatment?).
  • 3rd presented after fall against a wall discharged then represented with vomiting 2 hrs later and found to epidural needing needed treatment
  • 4th fall from a swing into a stream, returned 11 days later with continued headache and skull fracture. No treatment

PECARN

• Pediatric Emergency Care Applied Research Network
• Identification of children at very low risk of clinically important brain injuries after head trauma: a prospective cohort study. Kupperman et. al. Lancet. 374 (3), 1160-1170, 2009
• Objective: Derive and validate prediction rules for ciTBI to identify children at very low risk of ciTBI after blunt head trauma for whom CT might be unnecessary (included separate rule for <2 yo)
• Enrolled 43,904 pts from 25 US hospitals with 25% being less than 2 years of age
• Inclusions
  • < 18 yo
  • Presenting within 24 hrs
• Exclusion
  • Trivial injuries – ground level falls, walking/running into stationary objects (mild injuries) & no signs or symptoms of head trauma other than abrasions and lacerations
  • Penetrating trauma, known tumors, pre-existing neuro d/o, shunts, bleeding d/o GCS < 14
• Methods
  • Evaluated injury mechanism
  • Clinical variables
  • Rule derivation was determined by binary recursive partitioning….. ie decision tree
  • Preverbal (< 2yo) and verbal (>2yo) children were analyzed separately b/c of young pts greater sensitivity to radiation, decreased ability to communicate, and different mechanism and risks for TBI.
• Decision predictors <2yo
  • AMS
  • non-frontal scalp hematoma
  • LOC > 5 sec
  • severe injury mechanism
  • palpable skull fracture
  • not acting normally according to the parent.
• Decision predictors >2yo
  • AMS
  • Any lOC
  • Hx of vomiting
  • Severe injury mechanism
  • Clinical signs of basilar skull fracture
  • Severe headache
• Results
  • For pts < 2 yo — NPV 100% (1176/1176) and sensitivity of 100% (25/25)
  • For Pts > 2 yo — NPV 99.95% (3798/3800) and sensitivity of 96.8% (61/63)
  • Prediction rule missed 2 unhelmeted biker/inline skater –both large frontal hematoma and “moderate headache”? Neither required NSG
  • Believe PECARN to be most useful
  • Validated
  • Large study 44,000 US pts
  • Included different decision rule for children < 2
  • Fairly simple rules

This is an excellent 30,000 ft view of diaster medicine.

1. Disaster means demand > resources – goal is to keep it an ‘incident’ and not a ‘disaster’.
2. What constitutes a disaster may differ by facility, time of day, impact on the facility itself (damaged facilities or systems cannot take care of patients or keep staff safe as easily), and whether or not the incident impact is limited, or ongoing (bridge collapse vs. pandemic).
3. Incident management (Incident command system or ICS) is the way in which we coordinate the response resources to move from a reactive to a proactive phase, setting objectives to take control of the incident.
4. CO-S-TR is a framework for the early response to a major incident
   1. Command, control, communication, coordination (C4)
   2. Space, staff, stuff, special (Logistics)
   3. Triage, treatment, transport, tracking (Operations)
5. HICS (Hospital Incident Command System) is what we use as our ICS model.
6. Surge capacity is the ability to expand to meet larger than normal demand.
   1. Conventional capacity means usual beds in usual locations.
   2. Contingency capacity means functionally equivalent care provided in atypical locations (PACU, for example).
   3. Crisis capacity means we are stretching resources to the point where there is a risk to the patient of a poor outcome but it’s the best we can do in the situation (cot-based care, allocation strategies for medications, for example).
7. Key issues that arise in all incidents are communications and patient tracking.
8. After-action analysis helps identify issues that either went well (and why) and those that need to be improved (and how).

Compiled by Dr. John Hick, Medical Director for the Office of Emergency Preparedness with the Minnesota Department of Health.