Tag Archives: grover

Neuroleptic Malignant Syndrome

2 May

Overview:

-Occurs with start of a new psychiatric medication or dose adjustment; it is NOT associated with overdoses (usually at therapeutic level when levels checked)

-All of the atypical antipsychotics have been associated with NMS

 

Signs/Symptoms:

-Tetrad of fever, muscular rigidity, autonomic dysfunction, and altered mental status

-Rigidity usually cogwheel or lead-pipe rigidity

-Tachycardia

-Abnormal blood pressures (either high or low)

 

Labwork Findings:

-Elevated CK level

-Leukocytosis

 

Common Complications:

-Renal failure secondary to rhabdomyolysis

-Respiratory failure from muscle rigidity and altered mental status

 

Treatment

Supportive care and cessation of the antipsychotic medication is the primary treatment

-When intubating these patients, non-depolarizing agents such as rocuronium are preferred over depolarizing agents such as succinylcholine

-For sedation, benzodiazepines are the preferred medication treatment

 

Submitted by Joey Grover.

 

References: Tintinalli’s Emergency Medicine:  7th Edition; picture

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Esophageal Perforation

1 May

Common Causes:

-Iatrogenic causes are the most common (endoscopy, radiation, dilatations, variceal treatment)

-Boerhaave Syndrome

-Foreign body

-Trauma

-Tumor

 

Symptoms:

-Acute, severe chest pain usually most common

-Pain can radiate to the neck, abdomen, back, shoulders

-Symptoms are usually worsened with swallowing

 

Exam findings:

Cervical subcutaneous emphysema is common in upper (cervical) esophageal perforations

-Lower esophageal perforations often show no mediastinal emphysema

Hamman Crunch= Air in the mediastinum that is being moved by the beating heart

-Patients often develop pleural effusions

 

Boerhaave Syndrome

-Full thickness esophageal perforation

-Caused by sudden forceful rise in the intraesophageal pressure such as with sudden forceful emesis

-coughing, straining, seizures, and childbirth have all also been associated with it

-More often associated with distal esophageal perforations

 

Effects:

-Mediastinitis pneumonitis can lead to shock

-Proximal perforations are generally not as severe as distal perforations

-High mortality rate

 

Treatment:

Treat the shock

Broad spectrum antibiotics

Thoracic surgery consultation

 

Submitted by Joey Grover.

Sources: Tintinalli’s Emergency Medicine, 7th Edition; Image 

 

Guillain-Barre Syndrome (quick hits)

28 Apr

GBS:
-Primarily an acute inflammatory demyelinating polyneuropathy (AIDP)
-Often associated with prodromal infectious organisms:
            -Campylobacter jejuni (patients with diarrhea history)
            -CMV
            -EBV
            -Mycoplasma pneumonia

Cause:
-It is believed that macrophages attack antigens on the myelin sheath that are extremely similar to antigen on certain organisms
 

Symptoms:
Progressive, symmetrical distal weakness usually worse in the lower extremities (ASCENDING PARALYSIS)
-Associated with diminished DTRs
-Can affect all four extremities in up to 40% of cases
-Ocular muscles are usually spared in this disease 
 
Prognosis:
-Nearly one third require ventilator assistance during their course
-Peak disease severity is usually a weak after onset
 

Diagnosis:
-MRI imaging showing selective enhancement of the anterior spinal nerve roots
CSF fluid showing a very high protein with only a mild pleocytosis
-Electrophysiologic testing
 
Management:
Respiratory Assessment:
-FVC measurement is essential to determine the need for intubation/impending respiratory failure
-FVC less than 20ml/kg is associated with pending respiratory failure
-NIF less than 30cm H20 are also more likely to require intubation
 
Therapy
IVIG or plasma exchange are treatment of choices
 
Blood Pressure
-It is advised not to treat hypertension in GBS as the hypertensive stage is often followed by the hypotensive stage
 

Submitted by Joey Grover.
 References: Rosen’s Emergency Medicine: 7th Edition; picture

Hemolytic Uremic Syndrome

25 Apr

HUS:

-One of the most common causes for acute renal failure in children

-Mean age of presentation is between 3-5 years of age

 

Associated infections:

E. Coli 0157:H7 is the most common

-Shigella, S. pneumonia, and certain drugs are also associated with causing HUS

 

Concept of the Disease

-Fibrin strands form along blood vessels causing microangiopathic hemolytic anemia

-Renal dysfunction occurs directly from injury to the renal vasculature, as well as from platelet/complement deposit in the glomerular lumen.

 

Symptoms:

-Prodromic gastroenteritis:  Abdominal pain, bloody diarrhea

-Later effects:  Thrombocytopenia, microangiopathic hemolytic anemia, renal failure

 

Prognosis:

-Up to 25% of patients had long term renal injury

-Up to 12% of patients develop end stage renal disease or even death

-Recurrences are a possibility with a high mortality (up to 30%)

 

Treatment:

Gentle fluid resuscitation and supportive care

-Treatment of hyperkalemia when present

Transfusions as needed (platelet transfusions are reserved only in cases of bleeding)

-Antibiotics are not recommended for the gastroenteritis as they have been associated with increased release of verotoxin possibly increasing the risk for HUS

Plasmapharesis can be considered in severe cases

 

Submitted by Joey Grover. 

 

References: Rosen’s Emergency Medicine:  7th Edition.  picture

Epiglottitis (quick hits)

24 Apr

General:

-Also can be referred to as supraglottitis

Haemophilus influenza type b (cause approximately 25% of cases even now after vaccination), Staphylococcus and Streptococcus species are the most common causes

 

Features:

-Classic 3 D’s= Drooling, dysphagia, and distress

-Commonly describe worsening dysphagia, dysnpea,

-Fever, tachycardia, and cervical lymphadenopathy also presently common

-Insiratory stridor

-Patients often are sitting in the sniffing position to provide easier breathing

 

Diagnosis:

Xrays can be obtained which show “thumb sign”if you are really concerned about epiglottis and the patient is unstable, do any necessary imaging at the bedside

-Transnasal fiberoptic laryngoscopy is the imaging test of choice

-CT is not needed and should be avoided in any patient who develops worsening symptoms with laying down

 

Treatment:

-Supplemental humidified oxygen

-ENT consultation

-IV antibiotics (Ceftriaxone is first line drug)

-IV steroids

-ENT consultation

 

NOTE:  If intubation is needed, try performing awake fiberoptic intubation in the OR with tracheostomy equipment available if needed

 

Submitted by Joey Grover. 

 

References: Image: http://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/2011/nejm_2011.365.issue-5/nejmicm1009990/production/images/large/nejmicm1009990_f1.jpegTintinalli’s Emergency Medicine 7th Edition

Tranexamic Acid Use in Trauma

18 Feb

Pharmacology:

inhibits plasminogen activation thereby decreasing plasmin activity

Inhibits clot breakdown as opposed to new clot formation

-Excreted in urine

Half-life of 2 hours

 

Dosing:

1g loading dose over 10 minutes, followed by 1g over 8 hours

 

Data Behind its Use:

CRASH-2 Study

-looked at 20,211 trauma patients in 40 countries

-randomized double blinded placebo controlled multicenter study

-Primary outcome looked at was in hospital mortality

-Secondary outcomes included vascular occlusive events, transfusions, surgical interventions

Results:

Reduction in relative risk of all cause mortality (14.5% vs. 16%; p=0.0035) with a NNT of 67 trauma patients

Reduction in RR of death from bleeding of 15% (4.9% vs. 5.7%; p=0.0077)

-Benefits of TXA increased with administration within 3 hours and in hypotensive patients

-Death from head injury the same in both groups (previous studies showed not beneficial in SAH patients)

No significant difference in rate of vascular occlusive events (1.7% vs. 2.0%; p=0.084)

 

 Submitted by Joey Grover. 

 

Sources: Cap AP, Baer DG, Orman JA, Aden J, Ryan K, Blackbourne LH.  “Tranexamic Acid for Trauma Patients:  A Crticial Review of the Literature.” J Trauma.  2011;71:S9-S14.; CRASH-2 Trial Collaborators.  “Effect of Traneamic Acid on Death, Vascular Occlusive Events, and Blood Transfusion in Trauma Patients with Significant Haemorrhage (CRASH-2):  A Randomised Placebo-Controlled Trial.”  Lancet.   2010;376:23-32.; picture

Tetanus (quick review)

14 Feb

 -Caused from Clostridium tetani, a nonencapsulated anaerobic gram positive rod 

-Exist in either spore forming or vegetative state

 

-Once converted into vegetative form, it produces two exotoxins

1.  tetanolysin,  which helps spread the bacteria

2.  Tetanospasmin, responsible for clinical manifestations of tetanus

 

Effects of tetanospasmin:  

Acts on the motor end plates of skeletal muscle,

preventing the release of the inhibitory neurotransmitters glycine and GABA from presynaptic nerve terminals,

preventing normal inhibitory control of nervous system

 

-Overall features:  muscular rigidity, muscle contractions, autonomic nervous system instability

Incubation period is <24 hours to more than 1 month

 

-Types of Tetanus:

                1.  Generalized Tetanus

-Most common form (80% of cases)

Masseter muscle stiffness/pain (Lockjaw) most common complaint

-Shorter axon nerves affected first (facial muscles), with descending progression of the neck, trunk, extremities

-Transition of stiffness to rigidity leads to trismus and characteristic facial expression (risus sardonicus).

-Generally get dysphagia, arm flexing, wrist clenching, and lower extremity extension. 

-Autonomic disturbances include labile hypertension, hyperpyrexia, tachycardia, increased catecholamine release

                2.  Neonatal tetanus

-Frequently occur after unsterile treatment of umbilical cord stump with inadequately immunized mothers

-Generally present as weak, unable to suck, and irritable during 2nd week of life

                3.  Cephalic tetanus

                                -Generally occurs after head wounds

                                -Present with cranial nerve dysfunctions, traditionally cranial nerve 7

                4.  Local tetanus

                                -Rigidity of muscles near site of injury

                                -Resolves after weeks to months

-Diagnosed clinically

 

Treatment:

1.  Tetanus immunoglobulin– neutralizes circulating tetanospasmin.  Unknown dose needed but 3000 to 6000 units IM is recommended.  GIVE BEFORE WOUND DEBRIDEMENT .  Lasts in your system for 28 days so no need to repeat dosing

2.  Wound debridement- prevent further toxin production

3.  Metronidazole traditionally administered. 

4.  Muscle relaxants

5.  Autonomic dysfunction- Magnesium sulfate has been shown to decrease catecholamine release.  Labetalol can also be used.

6.   Active immunization- give them a TDAP

 

Submitted by Joey Grover.

 

Sources: Tintinalli’s Emergency Medicine:  7th Edition; Rosen’s Emergency Medicine:  7th Edition; picture