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Archive for January, 2011|Monthly archive page

Radiology: Ultrasound signs of Early pregnancy

In Uncategorized on January 27, 2011 at 4:58 am

**Quick Review**

When you have a pregnant female presenting with vaginal bleeding and/or abdominal pain, the most important diagnosis to exclude is an Ectopic pregnancy. About 1 in every 13 female presenting to the ED in their first trimester with abdominal/pelvic pain with or without vaginal bleeding will be diagnosed with an ectopic. You cannot decide NOT to do an ultrasound simply due to the B-HCG levels.

Remember – ‘discriminatory level’  is the level of HCG at which an IUP is expected to be visible. For transvaginal ultrasound its >1500mIU/ml, while for transabdominal ultrasound its >3000mIU/ml.

Signs of IUP in early pregnancy.

1. intradecidual sign – earliest sign but NOT a definate sign of an IUP. Its a thin walled anaechoic structure without a chorionic ring seen within the uterus.

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2. gestational sac with a yolk sac within the uterus = IUP

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3. at 6wks, a fetal pole and fetal HR should be visible; by 7wks, extremities should be visible and by 10wks(end of embryonic stage,

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Visit this site: http://www.sonoguide.com/obgyn.html

 

RSV

In EM2 on January 15, 2011 at 5:19 pm

2cases:

3 month old Male presenting with parents to the ED for cough x2days, congestion and one epeisode of vomitting. Parents denies fever, chills, sick contacts or other symptoms. Baby otherwise looks well, tolerating po and making wet diapers. immunizations UTD. Full term delivery, no complications at birth, on no medications otherwise. PE unremarkable, well appearing baby, Sa02 98% on room air. Labs: RSV+

Outcome: discussed with patient’s pediatrician, scheduled follow up in 2days, otherwise patient was dc’ed home with close instructions to parents to return if symptoms worsen or patient has trouble breathing.

4week old M brought into the ED with cough x3days, congestion and L eye crusting. [+]sick contacts but otherwise no complications at birth, full term, no medical hx or medications. PE shows mild bilateral conjunctival injection and oral thrush but otherwise good air exchange, SaO2 98% on room air, well appearing baby. Labs: RSV+

Outcome: transfered to children’s hospital for admission.

Teaching Point: When to admit for RSV infection

Overiew: RSV is a very common cause of upper respiratory track infection in infants and children during winter and spring months.  typically manifests as bronchiolitis or pneumonia. Spread via hand-hand contact, or contact with respiratory droplets (3-8dy incubation period). Typically presents clinically with cough, wheezing, decrease po intake.

Factors associated with more severe disease, thus supporting admission are:

age<3months at time of infection, prematurity (<35wks) at birth, children of multiple births(>3), oxygen saturation <95%, Toxic appearance on exam, RR>70 on room air, congenital lung or heart disease, neuromuscular disease, atelectasis or pneumonitis on CXR.

Management: If the baby is well appearing, well hydrated and tolerating PO intake without any of the factors listed above, management is typically symptomatic with close follow up in a few days with the patient’s pediatrician. Bronchodilators have not been shown to be particularly beneficial.

If the baby doesnot look well or have any of the factors above, then they should be hospitalized, and care is typically supportive as well (supplemental oxygen, IVF, bronchodilators). Aerosolized Ribavirin can be used in severe cases however its expensive and has not been shown to particularly reduce hospitalization or mortality. Typically, children hospitalized for RSV infection, do well and are discharged in a few days. They do have a higher incidence of subsequent wheezing in the future.

 

References:

Rosen’s 6th edition, chapter 128 pg 2051.

eMedicine: RSV (see link here)

 

Chapter Review: Hypothermia

In EM2 on January 9, 2011 at 11:12 pm

Physiology of Heat loss.

Core Body Temp is between 36.5-37.5C. Heat is lost via 4 main mechanism radiation, evaporation, conduction and convection. At cold temperatures (32-37C), the body attempts to generate heat primarily via shivering, but also with  vasoconstriction, increased catecholamine, thyroid and adrenal output. At T<32C, there’s loss of the shivering mechanism. At T<28C, loss of endocrine regulation and metabolic rate slows down by 50%.

Hypothermia: core Temp < 35C (95F)

Etiology: increased loss of heat (accidental heat loss, burns, iatrogenic), impaired thermogenesis(CNS impairment, trauma, ETOH)  or impaired thermoregulation(endocrine etiologies eg. thyroid). In the ED typically seen in age extremes, homeless people without adequate shelter, alchoholics.

Clinical

****get CORE temp with rectal, bladder or esophageal probe(low-reading temperature probe). NOT oral  or tympanic temp. Careful to ensure that you are not taking the temp of really cold stool 🙂 technically, the gold standard for getting the temp is with a pulmonary artery catheter – but this has obvious limitations.***

Mild Hypothermia (T: 32-35C) – tachypnea, tachycardia, shivering, ‘cold diuresis’, dysarthria

Moderate Hypothermia (T: 28-32C) – altered mental status, CNS depression, paradoxical undressing, hyporeflexia, Afib, bradycardia, slow respiratory rate

Severe Hypothermia(T<28C) –  hypotension, bradycardia, asystole/VF, coma, areflexia.

EKG: prolonged PR, QRS and QT intervals. + Osborn(J)waves. Classic progression is: bradycardia –>Afib –> slow ventricular rate –>V.Fib –>asystole

Workup :

no trends in electrolytes (watch for K 2/2 rhabdomyolysis or acidosis), hyperglycemia (insulin is inactive at T<30C)

H/H – hemoconcentrated – 2/2 diuresis, volume contraction and increase in HCT(by 2%) with every 1c drop in temp; leukopenia and thrombocytopenia may occure 2/2 splenic sequesteration.

Coags – hypothermia causes a prothrombotic state/DIC -picture likely 2/2 inactivation of coagulation cascade enzymes. Lab work may be falsely normal cause labs typically warm blood samples to 37C before running them.

CXR may show aspiration pneumonia, pulmonary edema.

Management – goal is T>32 at 0.5-2C/hour (or as fast as possible)

Think: is this patient mildly or profoundly hypothermic? what is their risk for cardiac dysrhythmia?

ABCDE – airway(intubate as indicated, provide warm humidified air either via ETT or Face mask), Breathing, Circulation (will likely require tons of warm(40-42C) IVF; low dose pressors may be indicated if refractory to fluid resuscitation but typically donot work until patient is rewarmed), Disability (GCS/intubate), Exposure(remove wet clothing, reduce agitation, keep patient warm and dry)

CPR: chest compressions should be held off if the patient has a frozen chest OR has any HR. With patient with a HR, chest compressions may agitate myocardium and lead to Vfib. Take 45-60sec palpating for a pulse before determining there is none and initiating CPR. Femoral access is the best option for central line access because there’s no risk of irritating the myocardium with the guidewire and the site is easily compressible.

Treatment of arrythmia: Defibrillation for VF and ACLS medication should be attempted ONCE but is pretty futile if core temp is <30C. Active rewarming should commence immediately if its unsuccessful. Atropine is typically not useful for bradycardia(since its not vagally mediated); Lidocaine is not typically useful for arrythmia. Bretylium has not been strongly proven to help.

Rewarming:

Passive External Rewarming – for mild hypothermia (therefore requires that the patient still has a physiologic response to cold to assit with rewarming measures). Remove wet clothes, Keep patient dry and warm with blankets. [results in core temp increase of 0.5-4c/hour]

Active external rewarming – bair hugger, warm IVF(you can heat up NSS to 40-42C – 1L bag for 2mins on high settings), hot water bottles at axilla, groin, extremities. [The bair hugger and similar gadgets typically cause about 1.5c/hr temperature increase]. Watch out for ‘Core temp afterdrop’ – occurs when trunk and extremities are rewarmed simultaneously, causing acidic cold blood in the extremities to return to the core and drop temp. Rewarming Shock – occurs when cold patient is removed from cold environment, causing peripheral vasodilation and shunting of blood from the core, resulting in hypotension.

Active Internal Rewarming : generally indicated in patients with hemodynamic compromise and/or ventricular arrythmias. Peritoneal dialysis with dialysate temp at 40-42C, heat irrigation(via thoracic lavage, NGT and [Foley with warm fluids – limited heat transfer 2/2 limited surface area]), Extracorporeal Blood rewarming (hemodialysis, cardiopulm bypass, Continuous arteriovenous rewarming, venovenous rewarming) – performed in cardiac arrest, when other measures have failed; warms at 2-4C/hr. CPB can rewarm up to 9.5c/hr!

Failure to rewarm(<0.6C/hr)? check and correct hypoglycemia(glu), AI (IV hydrocortisone), hypothyroid (IV levothyroxine), start empiric antibiotics (patient with hypothermia and sepsis have worse outcomes).

Further reading: the Jan 2011 Critical Decision Journal (from ACEP) has a great hypothermia write up – its emailed to EM residents for free. Check it out!

Chapter Review: Frost Bite

In EM2 on January 5, 2011 at 3:53 pm

Overview: Frost Bite is a dry cold related injury caused by freezing tissue. Typically seen in military/combat situations, homeless people, outdoor activity/athletics or in people with blunted self-protective instincts.

Pathophysiology: Cold temperature causes vasoconstriction and shunting of blood away from periphery towards the core to reduce heat loss. Tissue freezes at ZERO(0) degrees C. Frost bite injury occurs in 2phases:

  1. Ice crystal formation extracellularly causing extracellular fluid shift resulting in cell death once 1/3 of volume is lost.
  2. Stasis, sludging and cessation of blood flow. This could lead to microvascular collapse.

Clinical Presentation: 75% present with numbness. Patients also complain of clumsiness, heaviness/’clunk of wood’ sensation in extremities, pain, throbbing and electric-shock sensation in the affected part.

good prognosis: clear bullae, healthy appearing skin, positive sensation to pinprick

Poor Prognosis: ‘frostbite’ looking skin, hemorrahagic bullae, cyanosis.

4 degrees of injury:

  1. Erythema and anaesthsia
  2. Clear blisters, edema
  3. Hemorrhagic blisters, eschar formation in weeks
  4. full thickness injury involving muscles, bones and tendons

MANAGEMENT

General principles: keep affected area dry. remove all wet clothing. avoid vigorous rubbing. avoid partial rewarming: it’s better to transport a frozen part rather than initiate and then incomplete rewarming techniques.

ED management:

  1. Initiate rapid thawing by immersion of affected part in water at 40-42C (thermometer measured).  if >42C, may result in subsequent thermal injury.
  2. Provide parenteral analgesia during rethawing, it can be painful! Morphine or Toradol
  3. Rewarming typically takes 20-40mins and is complete when affected part ‘flushes'(erythema)
  4. Debride clear vesicles/blisters, LEAVE hemorrhagic blisters alone (since they represent damage to sub-dermal vasculature).
  5. Update Tetanus
  6. Consider IV PCN for strep prophylaxis in severe cases
  7. Check Labs- typically not helpful unless there’s underlying hypothermia, dehydration or sepsis from wound infection. Baseline Xrays should be obtained however Radiology is typically used if there’s suspected underlying fractures or dislocations.
  8. After rewarming, keep area dry and elevated.
  9. If Cyanosis persist after re-warming techniques, consider compartment syndrome (which may not be appreciated due to cold-induced loss of pain sensation)  as a diagnosis and measure compartment pressures.

Disposition: Most patients (except in mild cases) are admitted for 24-48hours. Surgical consult for long term management is warranted. Inpatient immersion hydrotherapy(baths) 30mins TID is typically indicated.

Frost bite injuries DONOT automatically warrant surgical management i.e. amputation. It takes up to 1-3months for viable tissue to heal and non-viable tissue to ‘declare’ itself. Think “Frostbite in January, amputate in July”. Recently due to advancement in radiologic evaluation of tissue, surgical decisions about grafts and amputations can be made in about 1 month. The amount of tissue eventually salvaged often exceeds even initial optimistic estimates

Sequelae are numerous including paresthesias, ‘electric-shock’ sensation, dermatologic changes, arthritis, muscular atrophy and many more.

High K

In EM2 on January 3, 2011 at 4:05 am

85 yo F, Hx dementia, CKD(no dialysis) presenting for repeat labs due to High potassium (7.1) on outpatient labs the day before. Patient has no complaint and is in no distress but with obvious dementia. Per daughter, Pt’s lives alone in an apartment with visiting nurses. Physical exam unremarkable asides from HR in 40-45, BP 142/80, afebrile, RR @ 12.

Positive Labs: K @6.0, trop  0.11; other electrolytes and blood count within normal.

3rd degree heart block

EKG: 3rd degree heart block

Outcome: patient was given IV calcium gluconate, insulin + dextrose, and kayexalate. Atropine was kept at bedside and pacer pads were place on. Patient remained asymptomatic while in ED. Cardiology was consulted for 3rd degree heart block. Discussions were underway to place a pacemaker.

Teaching Point: Manifestation and Management of Hyperkalemia

When you hear hyperkalemia + EKG, all medstudents and 1st yr residents can rant off ‘Tall-Peaked Twaves’ as the manifestation but there’s more to the EKG than this.

EKG progression of hyperK: Tall Peaked Twaves –> widening of QRS –>sine waves–>VFib or Asystole. Patients can get dysrhythmias including 2nd and 3rd degree heartblock and wide complex tachycardia. Clinical manifestations are typically neuromuscular including lethargy, weakness, areflexia and paralysis.

Management of hyperkalemia.

  1. Calcium gluconate – 10-20mL, IV, works to stabilize cardiac membrane, onset 1-3mins, duration about 30-60mins. Will typically give if EKG changes or K>6.0(anecdotal). NOT calcium carbonate (which is tums), NOT calcium chloride (which is about 10x more potent and is typically reserved for coding patients, unstable dysrhythmia or hypotension)
  2. Insulin + glucose – 10-20units IV regular insulin + Dextrose. causes cellular uptake of K+. onset at 30mins, duration 4-6hrs.
  3. Albuterol – nebulized albuterol 5-20mg, causes intracellular shift of K+, onset 30mins, lasts 2-4h.
  4. Kayexalate – 30G PO or PR, will facilitate renal excretion of K+. onset 1-2h, lasts 4-6h
  5. Dialysis – usually in unstable patients with hyperkalemia as a result of acute or chronic renal failure, rhabdomyolysis. works quick!
  6. Treat the underlying cause.