UMEM Educational Pearls

Myth: The ornamental red plant - poinsettia - gained a reputation as a poisonous plant from a case report. In 1919, a 2-year-old child reportedly died from an ingestion and later an 8-month-old developed mucosal burns.  These anectdotal case reports perpetuated the myth that poinsettia plants are poisonous. In the modern literature there is one single case of anaphylaxis(1) due to poinsettia ingestion/exposure, an allergic dermatitis(2) and one case of dermatitis(4). 

Krenzelok et al.(3) showed there were 22,793 cases of poinsettia exposure and there were no fatalities reported to poison centers. 96.1% were kept at home without sequelae.

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  1: Kimata H. Anaphylaxis by poinsettia in infants with atopic eczema. Allergy.  2007 Jan;62(1):91-2.     2: Bala TM, Panda M. No poinsettia this Christmas. South Med J. 2006  Jul;99(7):772-3.    3: Krenzelok EP, Jacobsen TD, Aronis JM. Poinsettia exposures have good  outcomes...just as we thought. Am J Emerg Med. 1996 Nov;14(7):671-4.     4: Edwards N. Local toxicity from a poinsettia plant: a case report. J Pediatr.1983 Mar;102(3):404-5.  

·      A parasitic disease transmitted by the bite of the 'Glossina' insect  (tsetse fly.)

·      The disease is most prevalent in rural areas of Africa. Untreated, it is usually fatal. Infection with the genus Trypanosoma brucei gambiense may lead to chronic asymptomatic illness.

·      Travelers to endemic areas in Africa are risk becoming infected.

·      Symptoms resemble a viral illness; headaches, fever, weakness, pain in the joints, and stiffness. The parasite is able to crosses the blood-brain barrier and causes neurological symptoms, mainly psychiatric disorders, seizures, coma and ultimately death.

·      Diagnosis is by serological tests (Card Agglutination Trypanosomiasis Test or CATT). Confirmation of infection requires the performance of parasitological tests to demonstrate the presence of trypanosomes in the patient.

·      Treatment: four drugs are registered for the treatment of HAT: pentamidine, suramin, melarsoprol and eflornithine.

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Management of patients with severe traumatic brain injury (TBI) typically involves the use of invasive intra-parenchymal pressure monitors. Although use of these monitors is recommended by TBI management guidelines, good quality evidence of benefit is lacking.

A recently published study evaluated the outcomes of TBI patients using a management protocol incorporating either an intracranial pressure (ICP) monitor compared to use of the clinical exam PLUS serial neuroimaging; a total of 324 patients were prospectively randomized into either group.

The primary study outcome was a composite of survival, impaired consciousness, and functional status at both three and six months.

The results of the study did not show a significant difference in the:

• Primary outcome  
• Median length of ICU stay
• Distribution of serious adverse events

Bottom line: This study suggests that clinical exam PLUS serial neuroimaging may perform as well as invasive intra-parenchymal monitors for guiding therapy in TBI patients.

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Question

50 year-old man with presents with acute-onset sharp left-sided chest pain and dyspnea. What's the diagnosis and the name of the abnormality on chest x-ray?

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• PAH can be classified as primary (PPH) or secondary pulmonary hypertension (SPH)
• Epoprostenol a prostacyclin analog was the first primary drug for patients w/PAH
• Recent clinical trials describe combination therapy as superior in efficacy to traditional monotherapy
• Varied etiologies of PAH hampers the performance of RCTs for each combination therapy
• PAH is associated w/diminished endothelium factor & nitric oxide, increased phosphodiesterase enzyme leading to the development of the ET-1 receptor antagonist (ERA) bosentan and the PDE- V inhibitor sildenafil
• RCTs are currently investigating the efficacy of three news agents in tx of PAH: imatinib, riociguat, and selexipag 

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Epistaxis can be a difficult thing to control in the ED, but there are several techniques you can learn that will make your life easier.

The majority of epistaxis cases are from kiesselbach's plexus therefore you can control it with:

Direct Pressure: Can be held with two fingers pinching the nares, or you can tape 4 tongue blades together and make your own "clothes pin" that can then be used to pinch the nares.

Vasoconstrictor and Anesthesia: A 1:1 mixture of topical lidocaine 4% and oxymetazoline can often be mixed together in the same oxymetazoline spray container enabling you to just spray it into the nares. This will often slow or stop the bleeding and provides anesthesia in case you need to cauterize the bleeding site.  Some IV/IM narcotic pain medication will also help increase patient cooperation.

Visualize the bleeding site: Use a HEAD LAMP with an appropriate sized nasal speculum. You may look like Marcus Welby, MD but nothing works as well to see into the nose.

Cauterization It is best to cauterize circumferential around the bleeding site prior to directly cauterizing the actual site. Be careful with electrical cautery so has not to perforate the septum.

Nasal Packing: Instead of using surgilube to lubricate the packing; use Muprion, Bactroban or Bacitracin ointment to lubricate the packing. This will reduce the chance of Toxic Shock Syndrome.

The more well known causes of toxin-induced hyperthermia include sympathomimetics and anticholinergics. In addition, neuroleptic malignant syndrome, serotonin syndrome, and malignant hyperthermia are high on the differential.

Several other xenobiotics can cause hyperthermia in overdose as well:

• Salicylates and dinitrophenol cause hyperthermia by uncoupling oxidative phosphorylation.
• Thyroid medications cause hyperthermia via thyroid hormone's thermogenic effect and psychomotor agitation. Hyperthermia can be extreme (>106°F, >41°C).
• Caffeine/theophylline, isoniazid, and strychnine cause hyperthermia through refractory seizures and muscle contraction. Highest temp recorded with strychnine is (109.4°F, 43°C).

In general, benzodiazepines should be considered first-line therapy, followed by barbiturates, propofol, or other sedative hypnotics. Phenytoin rarely has a role in the management of toxin-induced seizures. Extrenal cooling measures are also warranted. Specifically for isoniazid, pyridoxine should be administered immediately with a benzodiazepine.

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Background:

Dengue is the most rapidly expanding mosquito-borne virus with an increasing incidence and geographical area.  It is most commonly found in the tropics, but there are occasional outbreaks in other places, including Texas and Hawaii.

Clinical:

Three Phases:

1.  The febrile phase lasts 2-7 dyas and is similar to other viral syndromes, often with high fever and nausea/vomiting.  Petechiae may also be present which can be induced by the application of a tourniquet.

2. The critical phase occurs after defervescence and lasts only 24-48 hours. IT is marked by increased capillary permeability and can lead to severe pulmonary edema, shock, and multisystem organ failure.

3. The recovery phase is marked by hemodynamic improvement. Some patients have a rash described as "isles of white in a sea of red." 

Some patients will develop bradycardia. Most patients have a self-limited form of the illness that is not severe, and consists of symptoms seen in the febrile phase.  The patients that develop severe dengue can have markers in the febrile phase that are associated with organ dysfunction, GI bleeding, and increased capillary permeability. Other concerning symptoms early are abdominal tenderness and persistent vomiting.

Treatment:

Treatment is supportive, mostly consisting of IV fluids, which is very effective when started early in the patient's illness.  For more information and maps of endemic areas check out the CDC or WHO websites:  http://www.cdc.gov/travel/notices/in-the-news/dengue-tropical-sub-tropical.htm or http://www.who.int/denguecontrol/en/

University of Maryland Section for Global Emergency Health

Author: Jenny Saltzberg

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Ultrasound-Guided Pericardiocentesis

• Though emergent pericardiocentesis is a relatively rare procedure in the ED, it is a critical intervention in patients with effusion and life-threatening instability/PEA arrest.
• Ultrasound-guided pericardiocentesis is preferred over the traditional "blind" approach, as it allows the provider to choose an optimal position and is associated with fewer complications.
• A few pearls when using ultrasound for emergent pericardiocentesis:
  • Consider placing an NGT for abdominal decompression.
  • Don't mistake the epicardial fat pad for an effusion; fat pads don't change size and usually move in concert with the ventricle.
  • The apical 4-chamber view tends to be the most common probe position, as the largest collection of fluid is usually around the apex.
  • If you are unsure about your needle location, inject 5-ml of agitated saline to confirm you are in the pericardial space.

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Question

64 year-old male with no past medical history presents complaining of chronic weight-loss and diffuse chest pain; CXR is shown below. What's the diagnosis, and what other disease(s) may present this way?

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• Coarctation of the aorta (CoA) is the 5th most common congenital heart defect.
• CoA typically manifests as a discrete constriction of the aortic isthmus.
• The majority of patients affected present in infancy with varying degrees of heart failure, which reflect predominantly the severity of the aortic narrowing. 
• Some patients may not present until later in childhood or adolescence,  with upper extremity hypertension,  either due to less severe initial narrowing or to the development of collateral circulation bypassing the coarctation.
• Tx options include surgery, balloon angioplasty, and stenting.
• Although early surgery may prevent/delay the onset of hypertension, approximately 30% will be hypertensive by adolescence.
• HTN is the single most important outcome variable in patients with CoA
• HTN present in young children is often under-recognized or not treated aggressively enough, screening for cardiovascular & renovascular anomalies is essential  
• Untreated CoA has significant early mortality, with mean age of death ~30-40

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Are discharged patients who suffer minor thoracic injury at risk of developing delayed pneumonia?

Prospective study of 1,057 patients age 16 and older with minor thoracic injury who were discharged from the ED. 

32.8% had at least one rib fracture

8.2% had asthma

3.4% had COPD

Only 6 patients developed pneumonia!!

Sex, smoking, atelectasis on CXR, and alcohol intoxication were not significantly associated with delayed pneumonia.

However, for patients with preexistent pulmonary disease (asthma or COPD) AND rib fracture, the relative risk of delayed pneumonia was 8.6. Patients without either of these conditions are at extremely low risk of future development of pneumonia.  

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Epidemiology:

Trampoline injuries doubled between 1991 and 1996, increasing from 39,000 injuries per year to more then 83,000 injuries per year.  Injury rates and trampoline sales peaked in 2004 and have been decreasing since; however, hospitalization rates are still between 3% and 14%.

Risk Factors:

¾ of injuries occur when multiple people are on the trampoline at once

Smaller participants were 14x more likely to be injured then their heavier playmates

Falls account for 27-39% of all injuries

Springs and frames account for 20% of injuries

Up to ½ of injuries occur despite adult supervision

Injury types:

Lower extremity injuries are more common than upper extremity

Head and neck injuries accounted for 10-17% of trampoline injuries

Unique Injuries:

Proximal tibial fractures

Manubriosternal dislocations and sternal injuries

Vertebral artery dissection

Atlanto-axial subluxation

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• Serum total tryptase measurements may be useful for confirmation of venom or drug induced anaphylaxis (not as useful for food induced)
• Can send serial tryptase levels at the time of presentation, 1-2 hours later, and at resolution
• This is NOT helpful for confirmation at the time of the episode, as it takes several hours to perform

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40 yo previously healthy male in China who presents with prolonged “seizure” after receiving a cut on his foot while fishing 5 days ago.

Dx: Tetanus

Clinical features:

·      Incubation period 4-14 days

·      3 clinical forms:

1.     Local spasm

2.     Cephalic (rare) -  cranial nerve involvement

3.     Generalized (most common) - Descending spasm: facial sneer (risus sardonicus),   “locked jaw” trismus, neck stiffness, laryngeal spasm, abdominal muscle spasm.

·      Spasms continue to 3-4 weeks and can take months to fully recover

Complications: apnea, rhabodymyolysis, fracture/dislocations

Treatment: supportive, benzodiazepines, RSI, Tetanus IG (3000-5000 units IM), wound debridement

University of Maryland Section for Global Emergency Health

Author: Veronica Pei, MD

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Question

An 86 year-old nursing home resident presents to the ED with a urinary tract infection, four days after discharge from the inpatient service for the same diagnosis. She was discharged from the inpatient service with a prescription for ciprofloxacin to be given through her gastric feeding tube (she does not take anything orally). Could her tube feeds be playing a role in the relapse of her urinary tract infection?

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Question

11 year-old boy presents with right knee pain and swelling after falling off of his bicycle. What's the diagnosis?

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In the rare circumstance you need to treat a patient with suspected PID and an allergy to doxycycline, what is the alternative?

For oral regimens, azithromycin is an option in place of doxycycline.

• In one randomized trial, azithromycin demonstrated short-term effectiveness when given 500 mg X 1, followed by 250 mg/day for 6 days.
• In another randomized study, the combination of ceftriaxone 250 mg IM single dose and azithromycin 1 g orally once a week for 2 weeks was effective.

Suggested regimen for PID with doxycycline allergy:

• Ceftriaxone 250 mg IM X 1
• Azithromcyin 500 mg IV/PO X 1, then 250 mg PO daily for 6 days
• plus/minus Metronidazole 500 mg PO twice daily for 14 days

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It is not often that a CT will be able to give you a hint to a toxicologic diagnosis. The following are CT findings that are either suggestive and even sometimes almost diagnostic for a given to toxin:

1) Intraparenchymal or Subarachnoid Hemorrhage: sympathomimetics or mycotic anuerysm rupture secondary to IV drug abuse

2) Basal Ganglia bilateral focal necrosis: characteristic of carbon monoxide, cyanide, hydrogen sulfide and even methanol

3) Severe advanced atrophy out of proportion for age: alcoholism, toluene

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