SSRI Toxicity

Things to watch for in patients that are taking SSRI:

• Therapeutic administration usually safe
• Hyponatremia is a common adverse effect (ADH secretion regulated by serotonin)
• Serotonin Syndrome is a possibilty in combination with other serotnergic drugs
• One SSRI is more problematic than the rest => Citalopram and Escitalopram
  • The only SSRI that can cause QT prolongation (even 24hrs after OD) and can cause seizures
  • This is the only SSRI with significant toxicity and unfortunately is the most commonly Rx by psych

Don't forget to do  thorough assessment of deep tendon reflexes on physical examination when appropriate.  DTR assessment can help localize a lesion and determine a diagnosis (i.e. thyroid disease, Guillain Barre, spinal cord and peripheral nerve lesions).

DTR Assessment Scale:

• 4+ - very brisk, hyperactive with clonus<
• 3+ - brisker than normal
• 2+ - average, normal
• 1+ - somewhat diminished, low normal
• 0 - no response

Major DTR Assessment Locations:

• Triceps (C6, C7)
• Supinator or Brachioradialis (C5, C6)
• Knee (L2, L3, L4)
• Ankle (mainly S1)
• Plantar (L5, S1)

• Binding of vasopressor agents to their receptors is influenced by pH (and temperature and concentration)
• Acidic conditions have been shown to alter receptor numbers on cell surfaces as well as alter binding affinity
• Overall, pH values > 7.15 do not have an appreciable clinical effects on vasopressors
• At pH values < 7.1 reductions in effectiveness become apparent
• Routine administration of bicarbonate remains controversial
• Aggressively search for and treat the underlying cause of the acidosis

Blue Toe Syndrome

This syndrome refers to acute digital ischemia caused by athero-microembolism and is associated with cool, painful, cyanotic toes in the presence of palpable distal pulses.

Presence of this syndrome should prompt the Emergency Physician to search for the proximal source. Failure to identify the source and aggressively treat may lead to limb loss.

Common etiologies include:

• AAA
• Iliac artery aneurysm
• Popliteal artery aneurysm

Recent  studies have identified that a significant cause of morbidity and mortality in women, elderly, and patients with renal failure is the failure to consider renal insufficiency in dosing certain anticoagulants and anti-platelet medications, resulting in bleeding complications. Medications should be based on creatinine clearance, NOT SERUM CREATININE. When the creatinine clearance is < 30 mL/min, the dose of any renally-excreted medications should be decreased.

For example, an 85 yo woman that is 110 lbs and has a serum creatinine of 1.2 (sounds normal!) actually has a creatinine clearance < 30, which means that she has relative renal insufficiency. Her dosages of medications (e.g. enoxaparin) should be adjusted for this.

 Creatinine clearance can easily be calculated via computer programs that you can "google" (e.g. just google "creatinine clearance calculation"). If you enter the patient's gender, age, weight, and serum creatinine, the programs will calculate the value for you.

Placental Abruption

• Leading cause of fetal death (1-80 pregnancy)
• Evaluation
  • Ultrasound has very poor sensitivity
• Can check D-Dimer, Coags, Fibrinogen and Fibrin Split Products
• For a stable patient MRI can make diagnosis.
• Fetal monitoring (minimum four hours) where fetal distress and uterine contractions are seen.
• Risk factors for Placental Abruption
  • Hypertension
  • Pre-eclampsia
  • Diabetes
  • Trauma
  • Smoking
  • Cocaine
  • Advanced maternal age
• Treatment
  • C-Section

Pediatric Septic Shock

• Sepsis is the most common cause of pediatric deaths worldwide.
• Recognition is paramount!  Delayed Dx = Higher Mortality
  • Hypotension is a late finding. 
  • Look for other signs of End Organ Hypoperfusion
    • Prolonged Cap Refill, Change in MS
    • Tachycardia, Tachypnea
    • Elevated Lactate / unexplained metabolic acidosis
• Management strategy is similar to that of adults
  • Get access (Don’t forget your I/O’s if necessary)!
  • Fluid Resuscitation is the most important aspect of the management
    • Get 20-60ml/kg infused within the first 15 minutes
    • Children with septic shock who get >40ml/kg before the first hour have increased survival compared to those who do not.
      • They may require 60-200ml/kg over the first few hours.
  • Get your Abx on board quickly
  • Currently there are Protocols that are based on the Adult Surviving Sepsis Campaign.

Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics.  Pediatr Crit Care Med. 2005 Jan;6(1):2-8.

GHB

• Sedating and amnestic, has become notorious in chemical submission (date rape)
• Very fast onset and rapid resolution though respiratory depression can occur 
• Difficult to test for with few labs and quickly eliminated through urine 
• Best chance to catch it is if the patient's first urine void is collected and tested

According to ACEP's clinical policy, a non-contrast head CT is only indicated in mild traumatic brain injury under the following circumstances:  

1)  headache
2)  vomiting
3)  age over 60
4)  drug or alcohol intoxication
5)  short-term memory deficits
6)  physical evidence of injury above the clavicle
7)  seizure

A recent study came out which confirms what we already knew... that MRSA infections are no longer confined to ICUs but are spreading to the community. What the new study does show, is that it affects particular populations disproportionately and Baltimore City, more than any other study population. The full article is attached below, or can be obtained for free from the JAMA website.

"Unadjusted incidence rates of all types of invasive MRSA ranged between approximately 20 to 50 per 100 000 in most ABCs sites but were noticeably higher in 1 site (site 7, Baltimore City) (TABLE 2)." "... we calculated interval estimates excluding site 7 (Baltimore City) to allow the reader to interpret a range of estimates reflecting different metropolitan areas. Regarding the high observed incidence rates reported by site 7, we conducted an evaluation to determine whether these results were valid, including a review of casefinding methods, elimination of cases to include only those with zip codes represented in the denominator, contamination in any laboratory, and other potential causes for increased rates; however, none were in error."

Attachments

• 0710170948_jama_mrsa.pdf (129 Kb)

Hyperammonemia in the Critically Ill

• Patients with acute hyperammonemia have significant morbidity and mortality 
• Fulminant hepatic failure is the most common cause of acute hyperammonemia in adult ICUs
• Other causes include TPN, GI hemorrhage, steroid use, trauma, multiple myeloma, infection with urease-splitting organisms, and drugs (salicylates, valproate) 
• Cerebral edema, intracranial hypertension, seizures, and herniation are the most significant effects
• Initial management should focus on treating intracranial hypertension - mannitol, hypothermia, N-acetylcysteine have been used
• Lactulose has not been shown to reduce mortality in acute hyperammonemia but is unlikely to be harmful

Clay AS, Hainline BE. Hyperammonemia in the ICU. Chest 2007;132:1368-1378.

There is no good evidence for what type of workup an asymptomatic hypertensive patient should get in the ED.  An ECG is likely to show LVH, a cxr will be normal in most cases, and many patients will have some degree of proteinuria.

So, what is a safe and reasonable strategy to workup these patients?

• Consider checking a serum creatinine. I say consider because even this recommendation isn't terribly evidence-based. Elevated creatinine may NOT indicate that a hypertensive emergency is present, but if the creatinine is elevated it might persuade you to choose a different antihypertensive agent (HCTZ won't lower BP effectively if the creatinine near 2.0, and many of us would be a little hesitant to start an ACE-I if the creatinine is elevated). Although there is one study that showed absence of proteinuria and hematuria was correlated with a normal serum creatinine, many patients with asymptomatic HTN will have proteinuria.
• Repeat the BP several times. One study has shown that as many as 1/3 of patients with high BP in the ED do not have elevated BP when followed up as an outpatient. Many patients' BPs will spontaneously decline (regression to the mean).
• In the asymptomatic patient a CXR and ECG will likely not help you manage a patient, so don't waste your time and the patient's money getting it.

American College of Emergency Physicians 2006 Guidelines on the evaluation of asymptomatic HTN.

New onset atrial fibrillation is rarely the sole manifestation of myocardial infarction. In other words, in the absence of accompanying chest pressure, dyspnea, diaphoresis, or other anginal equivalents, a rule-out ACS workup in not supported by the literature and is not cost-effective.

The two exceptions to the statement above are elderly and diabetic patients, in whom subtle presentations of ACS are common with or without atrial fibrillation.

Pediatric Strain versus Fracture

• Due to the fact that tendons are much stronger than the physeal growth plate in pre-pubescent children, one should be extremely cautious when diagnosing a strain/sprain. 
• Pre-pubescent pediatric patients should be treated as if they have a Salter Harris I fracture with an appropriate splint and close follow up.

Review of Salter Harris Fractures

1. A fracture through the physeal growth plate. Typically can not be seen on x-ray unless they growth plate is widened.
2. A fracture through the physeal growth plate and metaphysis.
3. A fracture through the physeal growth plate and epiphysis.
4. A fracture through the physis, physeal growth plate and metaphysis.
5. A crush injury of the physeal growth plate.

Please click here for a pictorial of Salter Harris Fractures from FP Notebook.

Foreign Bodies
•    No object should be left in the esophagus for >24 hrs
•    Unusual FB’s:
        ==>    Very Sharp or pointed objects may perforate the GI tract and should be removed endoscopically.
        ==>    Long objects (>6cm) or wide (>2cm) objects may not pass and should  be remove  endoscopically.
•    Button Batteries
        ==>    9% of cases involve more than one battery (x-ray mouth to anus)
        ==>    Hazards:
                    (1)    Heavy metal leakage (Mercury) – low risk but real
                    (2)    Electrical Discharge (Local tissue injury)
                    (3)    Pressure Necrosis
                    (4)    Leakage of Corrosives
        ==>    85% Pass without symptoms
                    (1)    No intervention if pass the esophagus and pt is without symptoms

•    Consider Heliox as a temporizing measure in children with respiratory distress, while awaiting endoscopy/bronchoscopy.

Valproic Acid (Depakote) - Increased use for both seizure disorder, migraine prophylaxis and bipolar disorder - Causes hyperammonemia with or without hepatic insufficiency (Liver enzymes could be normal!) - Hyperammonemia can occur at therapeutic concentrations and overdose - If the patient is sedated and has hyperammonemia, consider carnitine therapy antidotal - Carnitine IV or PO: 50-100 mg/kg bolus or divided bid, safe to give

• The most common (80%) cause of non-traumatic subarachnoid hemorrhage (SAH) = ruptured saccular (berry) aneurysm.
• Saccular aneuryms are thought to be present in up to 5% of the population.
• There is a strong familial association with cerebral aneurysms, and prevalence is increased in people with Marfan Syndrome and Polycystic Kidney Disease.
• Other causes of non-traumatic SAH include:  AV malformation, cavernous angioma, mycotic aneurysm, and blood dyscrasia. 

[RESENT - STILL FIXING CODE - THESE TEST EMAILS SHOULD CEASE SHORTLY... SORRY FOR THE INCONVENIENCE]

• Abdominal compartment syndrome (ACS) is increasingly identified in the critically ill medical patient population
• ACS is defined as a sustained intra-abdominal pressure > 20 mmHg associated with new organ dysfunction
• Primary organs adversely affected by ACS include cardiac, pulmonary, GI, and renal
• To date, associated mortality rates have ranged from 27% to 50%
• Risk factors for ACS include:
  • massive fluid resuscitation ( >10 L crystalloid in 24 hours)
  • massive transfusion ( > 10 U PRBCs in 24 hours)
  • severe sepsis or septic shock from any cause
  • mechanical ventilation
  • PEEP > 10 cm H20
• Intravesicular (bladder) pressures are currently the standard monitoring modality
• Decompressive laparotomy is the current standard for management of ACS

Suspect an aortoenteric fistula in patients who present with an upper GI bleed if they have ever had a AAA repair. This occurs when a fistula forms between the abdominal aorta and the GI tract (most commonly the duodenum). Patients may present stable or may present critically-ill. Unstable patients with an upper GI bleed and a history of AAA repair should proceed to the OR for laparotomy.

Stable patient may undergo CT scanning and/or endoscopy. Bottom line: If a patient with a history of AAA repair presents with an upper GI bleed, rally your troops (GI, Surgery, etc) ASAP and don't mess around. If you are wrong, and the patient doesn't have a fistula, no big deal. If you are wrong, and the patient does have a fistula, the patient may very well die on you as you struggle to get a regular ICU bed.

In the treatment of an acute ST-elevation MI, there are three major signs of successful reperfusion:

1. T-wave inversion within the first 4 hours. If the T-wave inversions occur beyond 4 hours, it's uncertain.
2. Resolution of the STE by at least 70% in the lead with maximal STE.
3. Development of a "reperfusion arrhythmia," most notably accelerated idioventricular rhythm (AIVR), which looks like V.Tach but the rate is only 60-120. Remember, V.Tach should have a rate > 120.

Persistent pain/symptoms OR absence of STE resolution by 90 minutes warrants strong consideration of rescue angioplasty.