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
- A fracture through the physeal growth plate. Typically can not be seen on x-ray unless they growth plate is widened.
- A fracture through the physeal growth plate and metaphysis.
- A fracture through the physeal growth plate and epiphysis.
- A fracture through the physis, physeal growth plate and metaphysis.
- 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:
- T-wave inversion within the first 4 hours. If the T-wave inversions occur beyond 4 hours, it's uncertain.
- Resolution of the STE by at least 70% in the lead with maximal STE.
- 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.
Low Back is one of the most common complaints that we see in the Emergency Department. Our first priority is to rule out those causes that can lead to paralysis or death (i.e.: epidural abscess, pathological fracture, cauda equina syndrome, etc…). However, most of the back pain that we will see is musculoskeletal in origin.
- Routine imaging is not required. However, diagnostic imaging and testing should be obtained for patients with low back pain when severe or progressive neurologic deficits are present or when serious underlying conditions are suspected.
- For patients with low back pain, clinicians should consider the use of medications with proven benefits in conjunction with back care information and self-care. For most patients, first-line medication options are acetaminophen or nonsteroidal anti-inflammatory drugs.
- Medications that have good evidence of short-term effectiveness for low back pain are NSAIDs, acetaminophen, skeletal muscle relaxants (for acute low back pain), and tricyclic antidepressants (for chronic low back pain).
Links to the Clinical Guidelines are listed below:
- Evaluation and Treatment
- Nonpharmacologic Therapies for Acute and Chronic Low Back Pain
- Medications for Acute and Chronic Low Back Pain
Concussions
- Symptoms
- HA, Dizziness, Confusion, Tinnitus, Nausea, Vomiting, Vision changes
- 3 grades of Concussions
- Grade 1 = transient concussion symptoms. No amnesia. No LOC.
- Grade 2 = transient concussion symptoms with amnesia. No LOC.
- Grade 3 = + LOC of any durations
- Return to Play Guidelines
- (there is no consensus statement. What follows is based on the most conservative approach)
- Grade 1: Remove from game, Examine q 5 min.
Return to game when asymptomatic for 20 minutes. - Grade 2: Remove from game until asymptomatic for 1 week.
- Grade 3: ED evaluation. No contact sports for 1 month once asymptomatic for 2 weeks.
- These apply to first concussions. Increase concern with 2nd concussion.
- Second-Impact Syndrome
- Occurs when a player returns to contact sport before symptoms of 1 concussion have fully resolved.
- Even a minor blow to the head can result in loss of brain’s autoregulation of blood flow.
- Leads to vascular engorgement and subsequent herniation.
Colorado Medical Society School and Sports Medicine Committee. Guidelines for the management of concussion in sports. Colo Med 1990;87:4.
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| Notes to authors
|
dan
- Rubbing alcohol is 70% isopropanol, like drinking Bacardi 151 (151 proof)
- This is NOT a toxic alcohol in the traditional sense
- This causes a large ketosis, large osmol gap but NO anion gap and no acidosis
- This is because isopropanol is metabolized to acetone (a ketone) not an acid
- Toxicity: inebriation, hemorrhagic gastritis, sedation to the point of death/intubation
- Purulent nasal drainage for more than 10 days
- Or if symptoms less than 10 days and one or more of the following significant facial pain, facial/periorbital swelling, dental pain, or temperature greater than 39'C