Saturday July 19, 2008

Q: What is Jacksonian seizure?


A: Jacksonian seizure is an unique type of simple partial seizures in which symptoms start in one part of the body, then spread to another - "epileptic march". Abnormal movements may occur in the hand or foot, then move up the limb as the electrical activity spreads in the brain. People are completely aware of what is occurring during the seizure.

Jacksonian seizures are extremely varied and may involve, for example, apparently purposeful movements such as turning the head, eye movements, smacking the lips, mouth movements, drooling, rhythmic muscle contractions in a part of the body, abnormal numbness, tingling, and a crawling sensation over the skin. These motor symptoms spread slowly from one part of the body to another.

(These seizures are named after an english neurologist, John Hughlings Jackson who described it in 1863)

Friday July 18, 2008

Q: Which very commonly use drug in ICU may increase level of Fenoldopam by 30-70% when administered concurrently ?



Answer: Acetaminophen (Tylenol or Paracetamol)

Fenoldopam is a short-acting dopamine agonist (DA1) for management of severe HTN. It increases renal blood flow and sodium excretion. It is 10 times more potent than dopamine as renal vasodilator. Initial dose is 0.1-0.3 mcg/kg/min IV and should be increased cautiously to avoid reflex tachycardia in increments of 0.05-0.1 mcg/kg/min IV q15 min until target blood pressure achieved.

Fenoldpam is relatively contraindicated or should be used with caution in patients with glaucoma and angina. It may cause hypokalemia due to diuresis. Acetaminophen may increase levels by 30-70% when administered concurrently. Also beta-blockers increase risk of hypotension.

Thursday July 17, 2008

Q: Which drug can make Liver as enhanced on imaging?





Answer: Amiodarone

An unenhanced computed tomography (CT) scan will show a greatly increased density, due to iodine accumulation.



Recommended reading:

Hepatotoxicity during rapid intravenous loading with amiodarone: Description of three cases and review of the literature - Critical Care Medicine:Volume 33(1)January 2005pp 128-134

Wednesday July 16, 2008
Is enteral feeding is all we need in ICU???

It has been advocated for several years that one should start enteral feeding in intensive care unit as soon as possible. There are instances when patient is severely nutritionally depleted and enteral feeding may take a while, and is there any role for combination of enteral and parenteral feeding. Recent paper by Heidegger shed some light on it.

According to them, the evidence had shown that enteral nutrition can result in under-feeding and that nutritional goals are frequently reached only after one week. Contrary to former beliefs, recent meta-analyses of ICU studies showed that parenteral nutrition is not related to a surplus mortality and may even be associated with improved survival.

Conclusion: Early enteral nutrition is recommended in critically ill patients. Supplemental parenteral nutrition combined with enteral nutrition can be considered to cover the energy and protein targets when enteral nutrition alone fails to achieve the caloric goals. Whether this combined nutritional support provides any additional overall outcome benefit is yet to be determined. Further studies are suggested.


Reference: click to get abstract

Heidegger CP, Darmon B, Pichard CB. Enteral vs. parenteral nutrition for the critically ill patient: a combined support should be preferred. Current Opinion in Critical Care 2008; 14 (4): 408-414

Monday July 14, 2008
ARDS is ARDS !!

No! its no different or easy even if ARDS occurs due to extrapulmonary causes. See this study recently published in Chest 1.

Background: ARDS can occur from the two pathogenetic pathways: a direct pulmonary injury (ARDSp); and an indirect injury (ARDSexp).The metaanalysis was aimed at evaluating whether there is any difference in mortality between the two groups.

Methods: MEDLINE, EMBASE, and CINAHL databases were searched for relevant studies published from 1987 to 2007, and included studies that have reported mortality in the two groups of ARDS.

Results: 34 studies were find. In all, the studies involved 4,311 patients with

• 2,330 patients in the ARDSp group and
• 1,981 patients in the ARDSexp group

1. Mortality was similar in the two groups.
2. The mortality was no different whether the studies were classified as prospective or retrospective; small or large; or observational or interventional

Conclusions: The results of this study suggest that there is no difference in mortality between these two groups. Further studies should focus on specific etiologies within the subgroups rather than focusing on the broader division of ARDSp and ARDSexp.




Reference: click to get abstract

Is the Mortality Higher in the Pulmonary vs the Extrapulmonary ARDS?: A Metaanalysis Agarwal et al. Chest. 2008; 133: 1463-1473

Sunday July 13, 2008

Q; Which Venom poisoning is marked by following 10 clinical signs:

1. mydriasis,
2. nystagmus,
3. hypersalivation,
4. dysphagia,
5. restlessness (out of proportion)
6. bronchoconstriction,
7. bronchorrhea,
8. pharyngeal secretions,
9. diaphragmatic paralysis,
10. anaphylaxis

Hints: Its not a snake envenomation and signs occur within a few minutes after the sting


Answer: Scorpion Sting


See full review on Scorpion Sting (emedicine.com)


Will be available at our Toxicology / Drug overdose section

Saturday July 12, 2008
Colonic Necrosis - unusual complication of Kayexalate-Sorbitol

We are using sodium polystyrene sulfonate (SPS or Kayexalate) since last 45 years with great confidence. It is a common practice to add sorbitol to dissolve Kayexalate mainly to avoid fecal impaction or possible bowel obstruction. Kayexalate binds intraluminal calcium and may cause constipation, fecal impaction or bowel obstruction.

One of the relatively unknown complication of Kayexalate-sorbitol combination is colonic necrosis, although has been reported in literature earlier. The exact reason for colonic necrosis is not clear but the diagnosis can be made by the pathologic examination of post-operative specimen or material from endoscopic biopsy and may require specialized expertise and special stains. Sorbitol part is taught to be responsible for complication.Intensivist need to be wary of possible complication of acute abdomen after administration of kayexalate-sorbitol in 1% of cases, particularly in first 24-36 hours.

Friday July 11, 2008
Novoseven RT - New version of Novoseven (Recombinant Factor VII)

Novoseven RT is a new version or second generation of Novoseven (Recombinant Factor VII). RT stands for room temperature.

The new formulation allows the product to be stored at room temperature (up to 77 degrees Fahrenheit) for up to 2 years. NovoSeven RT contains sucrose and L-Methionine, which allow for storage at room temperature.

The original formula could be stored for three years at temperatures between 36 and 46 degrees Fahrenheit.


See Review and Recommendations for the Off Label Use of Recombinant Activated Human Coagulation Factor VII (Novoseven®) - VA MedSafe, Pharmacy Benefits Management Strategic Healthcare Group and the Medical Advisory Panel, February 2007 - pdf


Reference:

1. Novoseven RT - fda.gov

Thursday July 10, 2008

Q: You have been called to ED (emergency deptt.) to evaluate a patient with organophosphate poisoning. You determine patient need intubation to protect and avoid aspiration pneumonia. Which drug you would like to avoid during intubation process?



A; succinylcholine

Organophosphate poisoining is marked by "SLUDGE" like syndrome (Salivation, Lacrimation, Urinary Incontinence, Diarrhea, GI hypermotility) and Succinylcholine also increases salivation. Moreover organophosphate may potentiate effects of succinylcholine. Succinylcholine is relatively contraindicated in Organophosphate poisoining.

Previous ICU pearl: Accidental succinylcholine in pseudocholinesterase deficiency


For people interested in "collection", here is one article on succinylcholine written in 1956 and printed in CANADIAN ANAESTHETISTS' SOCIETY JOURNAL (Can. Anaes. Soc J., vol. 3, no. 1, Jan., 1956) - pdf file

Wednesday July 9, 2008
What if plasma exchange is not available as treatment of TTP

Q: You just diagnosed a patient with thrombotic thrombocytopenic purpura (TTP) but you were informed by the nursing supervisor that plasma exchange with fresh frozen plasma is not available in hospital due to technical reason and it will take time before patient can be transferred to a facility where the said services are available. What would be your alternate plan to bridge that time?

A; High-dose plasma infusion with rate of 25-30 mL/kg per day. When immediate plasma exchange with fresh frozen plasma is not available, simple plasma infusion can be performed until transfer to a higher facility is available. There is always a substanial risk of fluid overload with such high plasma infusion and you have to weigh risks and benefits of the clinical decision or to watch patient closely while plasma is infusing.


Reference: click to get abstract/article

High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome - Medicine. 82(1):27-38, January 2003.

Tuesday July 8, 2008
Corticosteroid and ARDS: Result of meta-analysis

Several articles have been written regarding role of steroids, its advantages or disadvantages in ARDS. Recently John Victor Peter and his group presented their findings in BMJ.

Method: Search of randomized controlled trials from years 1966 to april 2007.

Data extraction: Two investigators independently assessed trials for inclusion and extracted data into standardized forms. Differences were resolved by consensus.

Data synthesis: Nine randomized trials using variable dose and duration of steroids were identified. Preventive steroids (four studies) were associated with a trend to increase both the odds of patient developing ARDS (odds ratio 1.55), and the risk of mortality in those who subsequently developed ARDS (odds ratio 1.52).

• Steroid administration after the onset of ARDS (five studies) was associated with a trend in reduction in mortality (odds ratio .62).
• Steroid increase the number of ventilator free days compared to control (three studies, mean difference 4.05 days, 95% credible interval 0.22 to 8.71).
• Use of steroids was not associated with increase in risk of infection.

Conclusion: Role of use of steroids in ARDS is not clearly established. Preventive use of steroids increase the incidence of ARDS in critically ill patients, whereas use of steroids after the onset of ARDS possibly reduces the mortality and increases the ventilator free days.


Reference: click to get abstract

Peter JV, John P, Graham PL, Moran JL, George IA, Bersten A. Corticosteroids in the prevention and treatment of acute respiratory distress syndrome (ARDS) in adults: meta-analysis. BMJ 2008; 336:1006-1009.

Monday July 7, 2008
Is our ICU nurses sleepier then our floor nurses?

Recent paper published in Journal of Hospital Medicine from Surani and coll. helped to address this issue with their pilot study.

(Dr. S. Surani is co-editor of this website also)

METHODS: Post-night-shift nurses in the ICU and on general floors (medicine and surgery) were assessed using subjective (Epworth Sleepiness Scale [ESS]) and objective (Mean Sleep Latency Test [MSLT]) measures.

RESULTS:

• ESS was abnormal (>8) in 7 of 10 ICU nurses compared with 2 of 10 floor nurses (P < .005), and mean ESS score was also higher (8.7 ± 3.9 vs. 5.6 ± 2.1, respectively; P = 0.042).
• MSLT values for the first nap period were in the pathologic range in the ICU nurses compared with the floor nurses (4.65 ± 5.5 vs. 10.85 ± 7.4 minutes, respectively; P < .05).

CONCLUSIONS: Post-night-shift RNs working in the ICU have a pathologic degree of sleepiness.



Reference: click to get abstract

Surani S, Subramanyan S, Babbar H, Murphy J, Aguillar R. Sleepiness in critical care nurses: Results of a pilot study. Journal of Hospital Medicine 2008; 3(3):200-205

Sunday July 6, 2008

Q: Why we call it cryoprecipitate?

A: The name explains everthing. cryoprecipitate means "cold precipitate". When FFP is thawed slowly at 4 degree C, a white precipitate forms at the bottom of the bag, which can then be separated from the supernatant plasma. This precipitate is rich in fibrinogen, factor VIII, von Willebrand factor, factor XIII, and fibronectin - and call crayoprecipitate. One unit of cryoprecipitate is derived from fresh frozen plasma (FFP) prepared from a unit of whole blood and as it is only a little precipitate at the bottom of the bag, 1 unit of cryoprecipitate comprised only a volume of 10-20 mL. Contents:

• 80-100 units of factor VIII, which consists of both the procoagulant activity and the von Willebrand factor,
• 150-250 mg of fibrinogen,
• 50-100 units of factor XIII, and
• 50-60 mg of fibronectin.

Half life is about one year if stored at minus (-) 18 degree C. When ordered (generally given as 6 units at a time), cryoprecipitate is thawed back to 37 degree C. Once thawed it must be kept at room temperature and has an expiration time of 4 to 6 hours.

Saturday July 5, 2008
"estimated average glucose" (or eAG) instead of HbA1c?


Scenario: You admitted 38 year old female with DKA. Looking at her record, you found that her latest "estimated average glucose" reported is 212. What is her estimated HbA1C?

Answer: 9

The HbA1c measures blood glucose control over the previous 90 days. It is expressed as the percent of hemoglobin molecules that have glucose attached. Recommended goal is less than 7% for people with diabetes.

But a new study (soon to be published) has found a simple mathematical formula that can "translate" HbA1c levels into an eAG level. It almost accurately converted HbA1c levels into average glucose levels.

An "estimated average glucose" or eAG is an accurate and easier way to understand glucose control, and probably will soon become the standard of reporting blood glucose control .

Manual way to do formula is

28.7 x HbA1c - 46.7 = eAG (in mg/dl)

Or use following graph (HbA1C % is followed with both mg/dl and mmol/L values)

6 % = 126 mg/dl = 7.0 mmol/l
6.5% =140 mg/dl = 7.8 mmol/l
7 % = 154 mg/dl = 8.6 mmol/l
7.5 % = 169 mg/dl = 9.4 mmol/l
8 % = 183 mg/dl = 10.1 mmol/l
8.5% = 197 mg/dl = 10.9 mmol/l
9 % = 212 mg/dl = 11.8 mmol/l
9.5 % = 226 mg/dl = 12.6 mmol/l
10 % = 240 mg/dl = 13.4 mmol/l


Reference: Click to get abstract

Translating the A1C Assay Into Estimated Average Glucose Values - Publish Ahead of Print published online ahead of print June 7, 2008, findings will be printed in the August issue of Diabetes Care

Happy July 4


Patient: Tell me, doctor. Is it serious?
Doctor: Well, I wouldn’t advise you to start watching any serials on TV

Have a Great Bar B Q

Thursday July 3, 2008
Cardiac MRI to determine Myocardium Viability before revascularization

Even severely dysfunctional myocardium in patients with coronary artery disease may show functional improvement after revascularization. Recent literature is showing that Cardiac MRI (CMR) is superior to low-dose dobutamine echocardiography and thallium-SPECT for viability imaging.

The whole concept of viability on Cardiac MRI is based on the fact that all infarcts enhance vividly 10-15 minutes after intravenous contrast administration. Cardiac MRI shows the transmural extent of the infarct very reliably. It tells you that:

"white is dead" (All infarcts irrespective of age enhance)





In areas of hypokinesia, if there is a rim of "black" or non-infarcted myocardium that is not contracting well, it indicates the presence of hibernating myocardium, which is likely to improve after revascularization of the artery supplying that particular territory.

Viability imaging reliably allows identification of areas of hibernation and viable or non-viable myocardium. All infarcts irrespective of age enhance.

The percentage involvement of the myocardial wall thickness by an infarct determines viability. Involvement of the myocardium by more than 50% usually implies that there will be no improvement after revascularization And similarly, less than 25% involvement of the myocardium by infarction usually implies that there is an 80% chance of improvement after revascularization.

Read article CMR in Myocardial Viability (Reference: Bhavin Jankharia: CMR in Myocardial Viability. The Internet Journal of Cardiology. 2004. Volume 2 Number 2.)

Wednesday July 2, 2008

Scenario: You have a patient admitted with confirmed HIT (Heparin-Induced Thrombocytopenia). Patient was started on nonheparin anticoagulant (argatroban). Once platelet count reached a stable plateau and the INR (international normalized ratio) reached the intended target range, for how many days overlap of nonheparin anticoagulation and Coumadin should be continued? - Choose one

A) Switch immediately

B) 2 days

C) 3 days

D) 5 days




Answer: 5 days

According to new (june 2008) American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition) on Treatment and Prevention of Heparin-Induced Thrombocytopenia.

"For patients with strongly suspected or confirmed HIT, we recommend against the use of vitamin K antagonist (VKA) [coumarin] therapy until after the platelet count has substantially recovered (usually, to at least 150 x 109/L) over starting VKA therapy at a lower platelet count (Grade 1B); that VKA therapy be started only with low maintenance doses (maximum, 5 mg of warfarin or 6 mg of phenprocoumon) over higher initial doses (Grade 1B); and that the nonheparin anticoagulant (eg, lepirudin, argatroban, danaparoid) be continued until the platelet count has reached a stable plateau, the international normalized ratio (INR) has reached the intended target range, and after a minimum overlap of at least 5 days between nonheparin anticoagulation and VKA therapy rather than a shorter overlap (Grade 1B)".


You can read full guidelines here

Found full range of new ACCP GUIDELINES on ANTITHROMBOTIC AND THROMBOLYTIC THERAPY (8TH ED) here

Tuesday July 1, 2008
THAM

Introduction: In patients with acute respiratory distress syndrome (ARDS), permissive hypercapnia is a strategy to decrease airway pressures to prevent ventilator-induced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. A pure respiratory acidosis generally does not require alkali therapy. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on the type of acidosis, cardiorespiratory status, and lung mechanics.

Problem with NaHCO3: Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. But using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation.

THAM: Under above circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. Tromethamine (THAM) is a sodium-free alkalinizing agent that acts as a hydrogen ion (proton) acceptor. It is a weak base that combines with hydrogen ions from carbonic acid to form bicarbonate and cationic buffer. Administration of tromethamine decreases hydrogen ion concentration, which results in a decrease in carbon dioxide concentrations and an increase in bicarbonate concentrations. The administration of Tham also increases urine output through osmotic diuresis. Excretion of electrolytes and CO2 is also increased. Urine pH is raised along with the excretion of electrolytes.

Usual Dose:

Dose in ml's of 0.3M THAM = (1.1) (Wt. in Kg) (normal HCO3 – Pt’s HCO3)

OR

Dose in ml’s of 0.3M THAM = body wt in kg X base deficit in MEq/L x 1.1

Total dose should be administered over a period not less than 1 hour via central line. .3M THAM solution is available as premix and is contra-indicated in renal failure, anuria and hyperkalemia. It may cause transient hypoglycemia and respiratory depression.