Running diagnostics

Running diagnostics

Tuesday, June 27, 2017

Heat Exhaustion/Stroke

ER series 3 — Heat stroke

In the previous week we’ve been experiencing crazy good weather in Vancouver—so good that when I took a friend bike riding around Stanley Park, I got sunburnt on my face and arms! Crazy! Heat stroke seems like such a wimpy thing to get, but coming from Australia where it gets up to 40 degrees Celsius, heat stroke can be fatal; so we take heat stroke and sunscreen very seriously.

Most of time, people complaining about “getting heat stroke” are not actually getting heat stroke. Heat exhaustion is a step below heat stroke and affects young adults who overexert themselves, older adults who cannot dissipate heat at rest (for example, people who are on anticholinergic drugs such as antihistamines or tricyclic antidepressants), or people who are on neuroleptic drugs (for example, schizophrenics). Heat stroke refers to a life-threatening condition where the normal compensatory heat-shedding mechanisms fail.

Basically all the symptoms of heat exhaustion/stroke arise from depletion of water and salt from the circulating heat.


Exhaustion
Classic
Exertional
Clinical features
· Malaise, headache, fatigue
· Body temp <40.5°C
· Only signs of dehydration (increase HR, orthostatic hypotension)
· Occurs in high ambient temperatures
· Patients often older, poor, sedentary
· Dry, hot skin
· Body temp >40.5°C
· Altered mental status, seizures, delirium, coma
· May have elevated AST and ALT
· Occurs with high endogenous heat production and overwhelmed homeostatic mechanisms
· Patient often young and active
· Skin often diaphoretic
· Like classical heat stroke but may have DIC, ARF, rhabdomyolysis, marked lactic acidosis
Management
· Rest in cool environment
· Replace water loss PO slowly; normal saline IV for orthostatic hypotension
· Cool with water mist and standing fans
· Secure airway in case of seizure and aspiration
· Fluid resuscitation
· Ice water immersion only if closely monitored


Avoid epinephrine (which causes peripheral vasoconstriction) and antipyretics.

If patient doesn’t respond to therapy, look for other conditions that cause hyperpyrexia but NOT considered heat stroke:
·      Meningitis
·      Thyroid storm
·      Anticholinergic poisoning
·      Delirium tremens

·      Infection

If you would like to contribute to this topic or suggest other topics, please email me at musicdoctor.oli@gmail.com. This blog entry is also available in podcast form! Look for us on iTunes or at www.medonthego.podbean.com.

Friday, June 16, 2017

Eye Emergencies

 I have always felt that the eye has not been given the amount of time and detailed education that it deserves during med school training; and as a result, while doing my internship emergency rotation, every time a patient presents with an eye issue, I would secretly pray: “Please not me, not me…” So below are some general dos and don’ts when approaching the eye:
·      History and examination should include these aspects (PLOAFF):
o   Pupillary reactions
o   Lids and ocular adnexa
o   Ocular movement
o   Acuity
o   Fundus
o   Fields to confrontation
·      Never put pressure on the eye!
·      Never use atropine drops to dilate the pupil! Use short-acting mydriatic ONLY if necessary—and never when the ocular state/optic nerve function needs to be monitored.
·      X-ray the orbits when suspecting intraocular foreign body—request X-rays with eyes in up and down gazes.
·      Never use steroid drops in the emergency setting.
·      Do not apply ointment in cases suspected of having a penetrating injury.
·      Do not persist in removing a foreign body is it’s not easily removed.
·      Always provide systemic analgesia in cases of corneal injury.
·      Always pad an eye after instilling local anesthetic.
·      Always refer children with squints!

Regarding the use of a slit lamp, I’m kind of ashamed to say that I’ve only ever used it to check for corneal ulceration. I don’t really know all the other uses of the slit lamp and how to perform these tests; so I’ve looked up some useful videos which go through all the basics of the slit lamp use. (The third one is a gem.)

Moving on to some of the emergency presentations involving the eyes. These can be divided into approximately five big categories: foreign body, burns, trauma, painful red eye, and sudden loss of acuity.

Obviously, if there are foreign bodies within the eye, the goal is to locate and remove that object. Foreign bodies can be present in the lid, conjunctiva, cornea, and intraocular (remember to get that orbital X-ray!); they often cause abrasions too so check thoroughly with fluorescein. The main management is to rinse with lots and lots of saline, removal of foreign object, antibiotic drops qid, and tetanus prophylaxis.

The management of chemical burns is very similar to managing skin burns—first rinse and rinse with lots of saline! Local anesthetic and systemic analgesia can be used. Examine thoroughly to make sure all source of the chemical is removed. In thermal burns the principles are similar; start antibiotic drops and pad if possible. Flash burns can result from UV light, and the pain can start up to 6~12 hours after the injury and last for 24 hours; systemic analgesia, sedation, antibiotic ointment, and padding are usually needed.

Blunt force trauma can happen anywhere on the eye, and the history is not a good guide to the severity of the injuries—so beware! The key is to determine where the bleeding is! Although the subconjunctival hemorrhage looks really bad, it’s actually not that bad; only reassurance is needed. The hyphaema doesn’t look that bad in contrast, but it can cause secondary glaucoma; and there can be a more severe secondary hemorrhage 2~3 days later. This requires urgent ophthalmology consultation within 24 hours. Remember to avoid aspirin. Vitreous hemorrhage and choroidal hemorrhage also need consultation within 24 hours to exclude retinal detachment. The most urgent of all eye hemorrhages is the orbital hemorrhage, which usually is accompanied by blowout orbital fracture (RESTRICTION OF MOVEMENT AND DOUBLE VISION)—this is sight threatening and may need urgent decompression—especially if there is reduced vision, nonreactive pupils, or proptosis.

The painful red eye is a very scary topic. There are two ways of approaching it. The first way is to divide it into two big categories: inflammation or glaucoma. Inflammation would include acute conjunctivitis, acute keratitis (HERPES SIMPLEX ULCERATION), acute iritis (CILIARY INJECTION), and orbital cellulitis. Essentially the management is to swab the eye and start antibiotics/antiviral therapy; dilate the eye and give steroid drops for acute iritis. Acute narrow-angle glaucoma is sight threatening, so must be considered in all unilateral painful red eye. Tell-tale symptoms and signs are HALO AROUND LIGHTS, FIXED MID-DILATED PUPILS, nausea and vomiting, SHALLOW ANTERIOR CHAMBER, and increased intraocular pressure (>40mmHg). Treat with topical beta-blockers, adrenergics, and cholinergics and systemic carbonic anhydrase inhibitors and hyperosmotic agents. Refer urgently.

The second way to approach the red eye is by categorization of accompanying symptoms:
·      Light sensitivity—iritis, keratitis, abrasion, ulcer
·      Unilateral—as above + herpes simplex, acute angle closure glaucoma
·      Significant pain—as above + scleritis
·      White spot on cornea—corneal ulcer
·      Blurred vision—all of the above
·      Non-reactive pupil—acute glaucoma, iritis
·      Copious discharge—gonococcal conjunctivitis


Sudden loss of vision in a “white eye” usually means an occlusion of a blood vessel or retinal detachment. Retinal artery occlusion is usually painless, causing partial/total loss of vision, pale disc, retinal edema, CHERRY RED SPOT, and narrowed arteries; remember to investigate for the CAUSE such as temporal arteritis or emboli. Management includes lowering intraocular pressure (IV acetazolamide 500mg), dilate blood vessels by giving carbagen (95%O2 5%CO2) or rebreathing into paper bag, ESR levels, and urgent referral. Retinal vein occlusion can present also present as painless loss of vision, but there is usually dilated retinal veins with multiple hemorrhages through out retina and swollen disc. HISTORY OF FLASHES AND FLOATERS and partial field loss indicate retinal detachment; the retina is grey, elevated in a “veil-like” manner. Urgent referral needed. Another case to refer urgently is optic neuritis; the loss of vision is variable, but key symptom is CENTRAL FIELD LOSS, afferent pupillary defect, and marked loss of red saturation.

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Thursday, June 8, 2017

Hypertension Emergencies

As human bodies age, there is a natural “tendency” for increased levels: blood cholesterol levels, triglyceride levels, sugar levels…etc. Blood pressure is no exception, and hypertension is very common. One of my favorite medical facts is this: the most common etiology of essential hypertension is UNKNOWN! What makes it an emergency then? When the blood pressure is so high that there is life-threatening damage to end-artery organs. This is called hypertensive crisis or malignant hypertension and usually takes place when the blood pressure is at 180/115 or above. (Where there is no life threatening organ damage it is called hypertensive urgency.)

As the pressure starts damaging end-artery organs, symptoms will start to manifest:
·      Brain-related
o   Dizziness
o   Headache
o   Fatigue
o   Epistaxis
o   Flushed-face
o   Nervousness
·      Heart-related
o   Fourth heart sound and broad, notched P-waves on ECG
o   Echocardiographic evidence of left ventricular hypertrophy may appear later
o   Aortic dissection or leaking aneurysm may show up on CXR
·      Kidney-related
o   Polyuria/nocturia
o   Proteinuria
o   Microhematuria
o   Diminished renal concentrating ability
o   Nitrogen retention
·      Eye-related
o   Retinal hemorrhages/exudates
o   Papilledema

History and physical examination should be performed. Usually the blood pressure should be measured on two separate occasions, at least 3~5 minutes apart. But a very high reading (greater than or equal to 180/120) along with papilledema on examination constitutes as hypertensive emergency. Basic tests such as CBC, urinalysis, electrolytes and kidney function, and ECG should be ordered as well as more focused tests looking for specific causes of hypertension such as CXR and screening for pheochromocytoma.

Although most of essential hypertension is of unknown cause, there are a handful of diseases that will cause life-threatening hypertension:
o   Drugs! The use of sympathomimetic drugs such as cocaine and amphetamines can bring on severe hypertension. MAOI use with ingestion of tyramine-containing food (red wine and cheese—who knew my favorite combo can be deadly?) can also cause it.
o   Pheochromocytoma is a tumor made of chromaffin cells that secretes catecholamines—causing high blood pressure. Symptoms will include various combinations of headache, palpitations, tachycardia, excessive perspiration, tremor, and pallor.
o   Pre-eclampsia (140/100 or above PLUS proteinuria) and eclampsia during pregnancy (pre-eclampsia plus seizures). This can be life threatening for both mother and fetus, and deliver of the fetus is the definitive treatment.

Sometimes a disease does not lead to malignant hypertension but is so often associated with it that it really pays to check for these when a patient presents with severe hypertension:
o   Hypertensive encephalopathy—essentially, the blood pressure gets so high that cerebral autoregulation is lost, leading to vasospasms, which ultimately leads to ischemia.
o   Pulmonary edema—hypertension is often accompanied by left heart trouble (sometimes it may even be the cause of the trouble). Symptoms and signs of myocardial ischemia may be present.
o   Catastrophic intracranial event—anything from severe head trauma, ischemic stroke, SAH, or ICH can present with hypertension. This is the only setting where bringing down the blood pressure too quickly can be harmful, causing cerebral perfusion to drop. So a balance of sedation, analgesia, and antihypertensive care must be considered (maintain 150/100 for 5 days).
o   Thoracic aortic dissection—chronic hypertension is the underlying cause in 90% of cases. Patients can present with cardiac symptoms, and the telltale sign is DIFFERENTIAL ARM BP readings! CXR can show widened mediastinum. This is the only circumstance where rapid lowering of blood pressure to 110~120 systolic is done!

The general goal is to lower the blood pressure gradually over 24~48 hours (except for ischemic stroke), the 25% lowered in the first hour. The most common treatment is nitroprusside and labetalol. Glyceryl trinitrate is good if the patient also has myocardial ischemic symptoms. Hydralazine is used in pregnant women. Other anti-hypertensives such as ACE inhibitors are reserved for long-term blood pressure control.

This information is available in podcast form! Look for me at www.medonthego.podbean.com and stay tuned for more episodes!

Upper GI Bleeds

As always, this blog post is available in podcast form at www.medonthego.podbean.com. You can also find Med On The Go on iTunes and Google ...