This web site is intended for medical professionals working in an ICU or interested in Critical Care, but can also be accessed by the general public. The information provided here is made available for educational purposes only. The information given here is from textbooks/journals. I have provided the source, indicated references and given credit where applicable. Every post is linked to its source of information. Any kind of information posted on the web site is referenced and properly dated.

Monday, April 20, 2009

Quiz 3:





















Interpret the ECG? (click on the ECG to view a larger image)
 

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Answer to Quiz 2:

Ans: Anticholinergic syndrome by Jimson weed (Datura stramonium)

Discussion:

Other names: Datura Stramonium, Jimson weed, Angel’s trumpet, Apple of Peril, Jamestown weed, Thorn Apple, Talguacha.

It contains the Belladona alkaloids: Atropine (dl-hyoscyamine), Hyoscyamine, and Scopolamine (l-hyoscine).

One hundred of these seeds contain 6mg of Atropine. Other plant parts contain varying degrees of alkaloids.

It has been used since colonial times as both an herbal medicine and a drug of abuse.

Used theurapeutically as an asthama remedy or as a natural hallucinogen. May be mistakenly used in herbal teas.

The physical exam is consistent with anticholinergic poisoning.

Ingestion causes mydriasis, cycloplegia, dry skin and mucous membranes, anhydrosis, Flushed skin, Hyperthermia, tachycardia, hypertension, urinary retention, and ileus, confusion, agitation, disorientation and hallucinations.

Anticholinergic toxicity is described by the phrase,

As mad as a hatter,

as red as a beet,

as dry as a bone,

as blind as a bat,

and as hot as a hare.”

Onset of symptoms: 1-4 hours post-ingestion

Duration: Dose-dependent. Few hours to 2 weeks

Mechanism: Anticholinergic drugs or plants competitively bind to and block the muscarinic receptors.

Differential Diagnosis for the anticholinergic syndrome is broad and includes multiple plants (i.e. deadly nightshade), mushrooms, and drugs (i.e. diphenhydramine, phenothiazines).

A key feature that differentiates this clinical syndrome from sympathomimetic toxicity would be the absence of sweating, presence of urinary retention, and loss of bowel sounds.

Treatment:

Mildly poisoned: The majority of anticholinergic poisonings typically have good outcomes with simply supportive care along with benzodiazepines for agitation.

Moderate to Severe poisoning: In the extreme cases of poisoning with anticholinergic agents, patients can develop rhabdomyolysis, marked hyperthermia, and extreme agitation. Anticholinergic agents may also interfere with other receptors than just muscarinic receptors. For example, like cyclic antidepressants may inhibit cardiac sodium channels causing prolongation of the QRS complex, like phenothiazines may inhibit cardiac potassium efflux channels causing QT prolongation, and like diphenhydramine may inhibit histamine receptors resulting in seizures.

Treatment in such cases includes Intravenous Physostigmine (side-effect of physostigmine: seizures and dysrhythmias.

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Sunday, April 12, 2009

Quiz 2:




A 40-year-old male is brought by his wife to the Emergency Department that he was becoming markedly confused. According to his wife, this occurred after he ate the fruit given above.

The patient is agitated, following no commands, constantly moving in the stretcher, and talking with incomprehensible, mumbling speech. He is warm and dry to touch, no bowel sounds, pulse of 140 beats/minute, blood pressure of 160/90 mmHg, temperature of 38.4°C. He has dry chapped lips and fixed, dilated pupils. A Foley is placed with return of 1.5 L of urine.
What is the diagnosis?? Name the plant....

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Friday, April 10, 2009

Kerley's lines

Kerley A lines (red arrows): are a coarse network of essentially straight, linear opacities about 2 to 6 cm long and 1 mm thick within the lung substance usually situated in the upper zone and pointing toward the hilum centrally and directed toward but not extending to the pleural surface peripherally. The orientation of these lines does not conform to the distribution of the bronchovascular bundles; they represent edema of the central pulmonary septa and perilymphatic connective tissue. They are seen in pneumoconiosis, lymphangitic carcinoma, and pulmonary edema (in which case they may be reversible).

Kerley B lines (blue arrow): represent edema of the interlobular septa and are straight linear opacities approximately 1.5 to 2 cm in length and 1 to 2 mm in width situated at the lung base and oriented at right angles to the pleural surface.They are reversible and transient in pulmonary edema. They may be permanent and irreversible in chronic pulmonary venous hypertension, pneumoconiosis, sarcoidosis, and lymphangitic carcinoma.

Kerley C lines (green arrows): are reticular opacities at the lung base, representing Kerley’s B lines en face.These are usually septal lines and a specific feature suggesting lymphatic involvement.

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Thursday, April 9, 2009

The GRADE Criteria

Society of Critical Care Medicine’s rating system for references and recommendations:
Grades of Recommendation, Assessment, Development and Evaluation (GRADE) criteria:

References:
A - Randomized, prospective, controlled investigation
B - Nonrandomized, concurrent, or historical cohort investigation
C - Peer-reviewed, state-of-the-art articles, review articles, editorials, or substantial case series
D - Non–peer-reviewed published opinions, such as textbook statements or official organizational publications.

Recommendations:
Level 1: Convincingly justifiable on scientific evidence alone
Level 2: Reasonably justifiable by available scientific evidence and strongly supported by expert critical care opinion
Level 3: Adequate scientific evidence is lacking but widely supported by available data and expert critical care opinion

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Wednesday, April 8, 2009

Take care of ur mobile phones!


from www.cartoonstock.com

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Answer to Quiz 1:

ECG shows: a wide complex rhythm – with a sine-wave configuration – is sinoventricular rhythm.

Diagnosis: Hyperkalemia

More abt hyperkalemia:

Hyperkalemia is a common life-threatening metabolic emergency. It is most often diagnosed in patients with renal failure.

Hyperkalemia may present with lethargy and weakness as the sole manifestation; alternatively, the patient may demonstrate significant ECG abnormality in addition to the mental status and constitutional signs.

Pathophysiologically, increasing potassium levels are associated with depressed electrical conduction. Significant variation is noted with respect to serum potassium levels and clinical manifestation; in general, sudden or rapid increases in the serum potassium concentration are associated with earlier development of clinical illness, including ECG abnormalities. However, the relationship between potassium levels and ECG changes may vary between different patients.

K+ level = 5.5–6.5 mEq/L: Prominent T-wave; Tall, narrow, symmetric; Most prominent in precordial leads

K+ level = 6.5–8.0 mEq/L: Decreased P-wave amplitude; Prolonged PR interval; Prominent T-wave; QRS complex widening (minimal to sine-wave configuration); Dysrhythmia; Atrioventricular block; Intraventricular block; Bradycardia; Ventricular ectopy.

K+ level more than 8.0 mEq/L: Sinoventricular rhythm; Absence of P-wave; QRS complex widening, progressing to sine-wave QRS complex; Ventricular tachycardia; Ventricular fibrillation; Asystole.

The goals of therapy are a reduction of the serum potassium level coupled with a stabilization of the myocardial cell membrane.

The management of hyperkalemia includes therapies aimed at the stabilization of the myocardium (Calcium), temporary shifting of the excess potassium intracellularly (dextrose, insulin, beta-adrenergic agonists, magnesium, and sodium bicarbonate), and ultimate removal of the potassium from the body (gastrointestinal binding resins and hemodialysis).

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Monday, April 6, 2009

Quiz 1: Altered mental status with an abnormal electrocardiogram

A 30-year-old female presented to the emergency department with lethargy and weakness. Her past medical history and any further details regarding the current history of present illness were unavailable.
On examination, the patient was drowsy but arousable; vitals signs were: blood pressure 210/110 mmHg, pulse 70 beats/minute, and respirations 40/minute. The remainder of the examination was unremarkable except for an apparent A-V dialysis shunt in the left upper extremity. The electrocardiogram (ECG) is seen below:

What does the ECG show? What is your diagnosis?

 

 

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Thursday, April 2, 2009

International Surviving Sepsis Guidelines, 2008

Ref: Crit Care Med 2008 Vol. 36, No. 1;

Initial resuscitation (first 6 hrs)
● Begin resuscitation immediately in patients with hypotension or elevated serum lactate more than 4 mmol/L; do not delay pending ICU admission (1C)
● Resuscitation goals (1C)
- CVP 8-12 mm Hg (higher target CVP of 12–15 mm Hg is recommended in the presence of mechanical ventilation or preexisting decreased ventricular compliance.)
- Mean arterial pressure more than or equal to 65 mm Hg
- Urine output more than or equal to 0.5 mL per kg per hr
- Central venous (superior vena cava) oxygen saturation more than 70% or mixed venous more than 65%
● If venous oxygen saturation target is not achieved (2C)
- Consider further fluid
- Transfuse packed red blood cells if required to hematocrit of more than 30% and/or
- Start dobutamine infusion, maximum 20 microgm per kg per min

Diagnosis
● Obtain appropriate cultures before starting antibiotics provided this does not significantly delay antimicrobial administration (1C)
- Obtain two or more blood cultures
- One or more Blood Cultures should be percutaneous
- One BC from each vascular access device in place for more than 48 hrs
- Culture other sites as clinically indicated
● Perform imaging studies promptly to confirm and sample any source of infection, if safe to do so (1C)

Antibiotic therapy
● Begin intravenous antibiotics as early as possible and always within the first hour of recognizing severe sepsis (1D) and septic shock (1B)
● Broad-spectrum: one or more agents active against likely bacterial/fungal pathogens and with good penetration into presumed source (1B)
● Reassess antimicrobial regimen daily to optimize efficacy, prevent resistance, avoid toxicity, and minimize costs (1C)
- Consider combination therapy in Pseudomonas infections (2D)
- Consider combination empiric therapy in neutropenic patients (2D)
- Combination therapy for less than 3–5 days and de-escalation following susceptibilities (2D)
● Duration of therapy typically limited to 7–10 days; longer if response is slow or there are undrainable foci of infection or immunologic deficiencies (1D)
● Stop antimicrobial therapy if cause is found to be noninfectious (1D)


Source identification and control:
● A specific anatomic site of infection should be established as rapidly as possible (1C) and within first 6 hrs of presentation (1D)
● Formally evaluate patient for a focus of infection amenable to source control measures (e.g. abscess drainage, tissue debridement) (1C)
● Implement source control measures as soon as possible following successful initial resuscitation (1C) (exception: infected pancreatic necrosis, where surgical intervention is best delayed) (2B)
● Choose source control measure with maximum efficacy and minimal physiologic upset (1D)
● Remove intravascular access devices if potentially infected (1C)

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Wednesday, April 1, 2009

Joke of the week

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