Spontaneous bacterial peritonitis

An acute bacterial infection of ascitic fluid. Happens in people with ascites due to any etiology(even with CHF, Budd chiari !!!). The route of infection is still not entirely clear. It may be a simple translocation of bacteria from the gut due to bacterial overgrowth  (as previously thought), or from hematogenous spread. But in general its the gut bacteria which accounts for most of SBP. This is mainly due to reduced intestinal transit times in pts with cirrhosis, along with low protein and complement levels etc.
The common bugs are E.Coli, Klebsiella and Strep pneumoniae.
Diagnosis is based on diagnostic aspiration of the ascitic fluid. We all tap the ascitic fluid in someone with symptoms of infection(fever, abdominal pain, tenderness etc). But around 30% of pts with SBP might not have any symptoms!! So...what shall we do?.........One of our gastroenterologist says...."JUST TAP ALL ASCITES". Well...he might be right...given a mortality range of 30-70% for SBP!


Based on the tap....it can be classified as follows...
1.SBP - if >250 PMN/micL  AND positive culture.
2.Culture-negative neutrocytic ascites -ascitic fluid culture is negative, but PMN count is ≥ 250 cells/µL. 
3. Monomicrobial nonneutrocytic bacterascites - positive culture result with a PMN count ≤ 250 cells/µL.
Irrespective of what type it is!!!......they all need to be treated based on clinical suspicion.


A very simple method being used these days(mostly in Europe) to diagnose SBP is the simple Leukocyte esterase test, which can be done at bedside. It has a sensitivity & specificity of 100 % & 91% resp to diagnose SBP! ( E Jof Gastro Hep 2007)
What to treat with -- A 3rd generation Cephalosporin or a fluroquinolone. Its rare to have anaerobic SBP , as ascitic fluid is rich in Oxygen!


When to use albumin - One of the main causes of mortality in SBP is due to development of renal failure. Albumin in addition to antibiotics have shown to prevent renal impairment and also to reduce mortality by around 10 to 15%based on this randomised trial(NEJM 1999). Its given as 1.5 g/kg at diagnosis and 1 g/kg on Day3.There is another randomised trial underway in Brazil to add more evidence to this practice.(ALTERNATE trial). 


Prohylaxis for SBP - Well..there are a group of patients who will benifit from prophylaxis. They are 1.anyone with a previous episode of SBP reducing mortality by 25% over a 1 year period(Hepatology 1990)  2. GI bleed with a course of 7 days.  3.pts with ascitic fluid protein <1 g/dl plus one of the following --- creatinine >1.5, bilirubin>4.(Hepatology 1995) The last criteria is a soft call, and would depend on local practice.The last two indications are a short course(1 -2 weeks) of antibiotics.The first indication is a longer term prophylaxis (1 year or more). Norfloxacin 400 daily is a preferred drug(as it selectively targets Gram negatives, and leaves anaerobes !)

Iron and Iron defeciency anemia - quick recap

Eventhough we have read about Iron deficiency and anemia for a while now, we kind of need some reinforcements from time to time.(I....definitely need some!!). 
Lets start with the iron  panel (well ...never forget to examine and correlate with the pt history & findings!)

IRON PANEL - A normal adult body contains 3-4 grams of iron; about 2 grams is stored in hemoglobin, about 400mg in iron-containing proteins, about 3-7 mg is bound to transferrin in plasma, and the remaining iron is stored as ferritin and hemosiderin (an iron storage complex found within cells). Transferrin saturation(TSAT) & total iron binding capacity(TIBC) are 2 common tests done. TSAT essentially measures the same thing as TIBC. Total iron binding capacity indicates how much room there is for iron, while TSAT shows how much iron is currently saturating transferrin. Usually transferrin is about 1/3 full of iron: serum iron (Fe) divided by TIBC = 1/3. TSAT is reduced in patients with IDA and often in patients with anemia of chronic disease.

Ferritin is the cellular storage protein for iron in tissues found in the intestines, liver and spleen which contain approximately 20% iron.In general, TSAT < 20 &/or ferrtin<200ng/dl are considered to be iron deficient.


CALCULATE IRON DEFICIT - (especially if rapid replenishment is planned) - First, calculate the patient’s hemoglobin deficit by subtracting their current hemoglobin from the goal of 14g/dL. Second,calculate the body’s total hemoglobin deficit in grams by multiplying pts. weight by the normal blood volume of 65mL/kg.Tis gives the total hemoglobin deficit.There are 3.3mg of iron for each gram of hemoglobin in the blood. So,lastly, multiply the total hemoglobin deficit by 3.3mg to calculate iron deficit. 


SOME FACTS ABOUT ORAL IRON REPLACEMENT

*The recommended daily dose for the treatment of IDA in adults is 150-200 mg per day of elemental iron.(a 325mg FeSo4 tablet has 65mg iron, a 325mg ferrous fumarate has 106mg of iron)
*It is best to give iron on an empty stomach ...as otherwise the iron binds with food in the stomach and impair
absorption; additionally, iron is best absorbed in an acidic environment.
*Since Iron is absorbed in the duodenum, enteric coated tablets may not be useful.
*After initiating oral iron, reticulocytosis will peak at 7-10 days in patients with moderate to severe anemia. *Hemoglobin levels begin to rise in 2 weeks. If taken in adequate doses, the hemoglobin would normalise by 8 - 10 weeks.
*10 to 20% of patients will have GI side effects. So, a tablet with lower elemental iron may be tried.....or tablet may be tried with a small snack(accepting a somewhat reduced absorption)

VRE ...when to treat!!

Vancomycin resistant enterococci are emerging as another leading nosocomial bacteria in hospitals.Enterococci are gram-positive and facultatively anaerobic microorganisms commonly found as part of the normal flora in the gastrointestinal tract.Several factors contribute to this increased risk among hospitalized patients, such as the disruption of the normal gastrointestinal flora by administration of broad-spectrum antibiotics, colonization with hospital-associated strains, poor infection control practices, presence of indwelling devices including urinary catheters, and an immunosuppressed state.Enterococcus faecalis andEnterococcus faecium are the two most common species isolated in this setting. The most common types of infection caused by enterococci are urinary tract infections (UTIs)


Given this intro...there may be 3 clinical scenarios we come across in hospital practice...
1. VRE UTI                 2. aymptomatic VRE bactereuria         3.VRE colonization
Well ..these have to be differentiated in clinical practice, as the last 2 dont need treatment , except in some special circumstances.

 A good detailed history about UTI symptoms in very much the deciding step for who to treat. Any lower or upper UTI system is needed to suspect UTI from VRE( except in elderly pts ). Once this is present, then proceed according to the flow sheet above.Evidence of VRE in the urine in the absence of symptoms or pyuria may have limited clinical importance in most patients, representing asymptomatic VRE bacteriuria or colonization, and generally does not require treatment; however, treatment may be considered in very high-risk patients (e.g., patients with catheter-acquired bacteriuria that persists 48 hrs after indwelling catheter removal, patients with planned genitourinary procedures, solid organ transplant recipients, neutropenic patients, and pregnant women).Always change Foley catheters once VRE is found in the urine.


 Aminopenicillins, both with (e.g., ampicillin-sulbactam, amoxicillin-clavulanate) or without β-lactamase inhibitors and penicillin are generally considered to be the drugs of choice for the empiric treatment of VRE infections.In case of ampicillin resistance , then nitrofurantoin or Linezolid can be used for VRE cystitis...........and Daptomycin or Linezolid can be used for upper tract UTIs and VRE bactermia. Duration of treatment doesnt need to be extended beyond 14 days.

The masks we (throw) use on patients .......

Oxygen masks are effective oxygen delivery device which is used mainly to supply oxygen from a storage tank to the lungs. Many people make use of this nowadays most especially medical care providers, aviators, medical researchers and hyperbaric chamber and other patients. Because of this, a wide variety of styles are now available for oxygen masks.

There are four available basic styles of oxygen masks. These are the simple facemask, the venture mask, the partial rebreather mask and the non-rebreather mask.

The simple facemask is the most commonly available oxygen mask to the public. This has a number of vents on both sides and can deliver 35-40 percent of oxygen. However if the oxygen flow increases to 10L/min, this can deliver up to 50 percent oxygen. The disadvantage with this type of oxygen mask is that this seals poorly and has large ventilation holes, thus oxygen flow is diluted with air.

The venture mask, on the other hand, is an oxygen mask that uses a mechanical venturi effect in order to increase the flow rate of oxygen into the mask. It supplies a desired amount of oxygen starting from 24% upto 40%, and this amount can be adjusted by using different valves. Useful in COPD patients when you want to control the amount of O2 they receive.

Another type of oxygen mask is the partial rebreather. This type of mask, which is often called as medium concentration oxygen delivery mask, almost looks like the non-rebreather mask but it does not have a one-way valve between the mask and the reservoir bag. This delivers almost 40 to 50 percent oxygen, and can increase up to 60 percent. Dont use this in a patient with tendency towards Co2 retention.

The last type is the non-rebreather. From the four types, this is the one that can deliver up to 90 percent of oxygen. This makes use of valves on both sides in order to prevent air and patient exhalation from diluting the oxygen in the reservoir bag. The valves open when the patient inhales and breathes in oxygen. However, masks of this type with valves on both sides are prescription masks only.

These are the different styles of oxygen masks. All are able to deliver the amount of oxygen needed. These are effective if used in appropriate clinical setting!!

Calcium gluconate in a digitalised heart with hyperkalemia! OK...or..NOT OK???

Today's morning report was about a young guy who was admitted with rhabdomyolysis, renal failure and hyperkalemia(K- 12mEq/dl) with sine wave pattern on his EKG. All this was due to a electrocution injury.So ...going through the management of hyperkalemia, someone pitched in the problem of giving Calcium gluconate in patients on Digoxin. Well....we had a couple of explanations for the interaction.So lets review the problem with these two drugs together.
First.....the mechanism of action of Digoxin- Digoxin inhibits the Na⁺/K⁺-ATPase(exchanges 2 K for 3Na) in the cardiac myocyte by competing with potassium,and causes intracellular sodium concentration to increase. This then leads to an accumulation of intracellular calcium by blocking the Na⁺-Ca⁺⁺ exchange system. In the heart, increased intracellular calcium causes more calcium to be released by the sarcoplasmic reticulum, thereby making more calcium available to bind to troponin-C, which increases contractility (inotropy).


Second.....the mechanism of action of Calcium gluconate- a litlte more cellular pathology! . Normally the cardiac myocyte has a resting membrane potential(RMP is -90mV) and a threshold potential at which it is excited(TP is-75mV).So a 15mV depolarisation is needed to excite the myocyte. In hyperkalemia, the RMP becomes less negative (-80mV) , but the TP remains at -75mV. This means that ..now..only a 5mV depolarisation is enough to excite the myocyte. This is the cause of hyperexcitability leading to arrhythmia.Calcium gluconate...by increasing Ca transport across the membrane reduces the TP from -75mV to around -65mV ...restoring the 15mV depolarisation needed to excite the myocyte. (the numbers in mV are just an example)  ...... Annals of Emer Med 2011


Sooo...in patients on Digoxin(which causes positive inotropy through calcium)...if more calcium is given....it can lead to more intracellular calcium in mycocyte leading to what has been described as cardiac tetany due to prolonged depolarisation. So ,does hyperkalemia make this process worse?? Well, probably not. ------Since K+ and digoxin compete for Na/KATPase, the binding depends on the concentration of the two. In hyperkalemic state...K+ binds preferentially than digoxin, on Na/K ATPase, and thus resulting in diminished digoxin action. (to better understand...think about hypokalemic states...where digoxin will bind preferentially to the receptor, and hence result in digoxin toxicity!--which is well known)
A slightly different scenario would be...when some one(with no K+ problems) takes too much digoxin...which will also result in digoxin binding preferentially than K+,  to Na/KATP ase resulting in Dig toxicity. In this setting....pt may go hyperkalemia..as more K+ ends up extracellularly (due to not binding with Na/K ATPase), and if this patient gets Ca gluconate..then again..it can causes arrhythmias.


Bottom line is...if Calcium is given(and pt made hypercalcemic) to any pt on Digoxin ..there is a increased possibility for cardiac arrhythmias(PG Med J 1999) ...irrespective of whether they have hyperkalemia or not. 
Whether these pathophysiologies!! are clinically relevant is not clear, as these interactions are based on few case reports only. Have a look at this animal study (J clin Tox 2004) and this retrospective study on pts ..over 18 years from a hospital in Arizona(J Emer Med 2011).Both of them show no clinically relevant interaction of Calcium administration even in Digoxin toxicity.     !!!!!!!

Some key aspects of Surviving sepsis

The key recommendations covering all aspects of sepsis treatment were outlined in the 2008 update on Surviving sepsis campaign. This is a tribute to my 2 month CU rotation which I completed this week.....


Early goal-directed resuscitation of the septic patient during the first 6 hrs after recognition (1C)
Blood cultures before antibiotic therapy (1C);
 Imaging studies performed promptly to confirm potential source of infection (1C); 
Administration of broad-spectrum antibiotic therapy within 1 hr of diagnosis of septic shock (1B) and severe sepsis without septic shock (1D);
 Reassessment of antibiotic therapy with microbiology and clinical data to narrow coverage, when appropriate (1C); a usual 7–10 days of antibiotic therapy guided by clinical response (1D);
 Source control with attention to the balance of risks and benefits of the chosen method (1C);
 Administration of either crystalloid or colloid fluid resuscitation (1B);
 Fluid challenge to restore mean circulating filling pressure (1C); reduction in rate of fluid administration with rising filing pressures and no improvement in tissue perfusion (1D); Vasopressor preference for norepinephrine or dopamine to maintain an initial target of mean arterial pressure ≥65 mm Hg (1C); dobutamine inotropic therapy when cardiac output remains low despite fluid resuscitation and combined inotropic/vasopressor therapy (1C);
 Stress-dose steroid therapy given only in septic shock after blood pressure is identified to be poorly responsive to fluid and vasopressor therapy (2C); 
Recombinant activated protein C in patients with severe sepsis and clinical assessment of high risk for death (2B except 2C for postoperative patients).
 In the absence of tissue hypoperfusion, coronary artery disease, or acute hemorrhage, target a hemoglobin of 7–9 g/dL (1B);
 A low tidal volume (1B) and limitation of inspiratory plateau pressure strategy (1C) for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS); 
Application of at least a minimal amount of positive end-expiratory pressure in acute lung injury (1C); head of bed elevation in mechanically ventilated patients unless contraindicated (1B); avoiding routine use of pulmonary artery catheters in ALI/ARDS (1A);
 To decrease days of mechanical ventilation and ICU length of stay, a conservative fluid strategy for patients with established ALI/ARDS who are not in shock (1C);
 Protocols for weaning and sedation/analgesia (1B); using either intermittent bolus sedation or continuous infusion sedation with daily interruptions or lightening (1B); avoidance of neuromuscular blockers, if at all possible (1B);
Institution of glycemic control , targeting a blood glucose <150 mg/dL after initial stabilization (2C);
 Equivalency of continuous veno-veno hemofiltration or intermittent hemodialysis (2B); 
prophylaxis for deep vein thrombosis (1A); 
Use of stress ulcer prophylaxis to prevent upper gastrointestinal bleeding using H2 blockers (1A) or proton pump inhibitors (1B); and consideration of limitation of support where appropriate (1D).


Our hospital has a Sepsis alert system whereby anyone getting into ER with tachycardia and fever will be eligible for a STAT call to the ICU resident (which was unfortunately 'I' for the last 2 months!!). http://www.survivingsepsis.org/About_the_Campaign/Documents/Final%2008%20SSC%20Guidelines.pdf

complications during rewarming

Therapeutic rewarming is being used widely in patients after a cardiac arrest (irrespective of type of cardiac arrest). Earlier the patient is cooled ..better the neurological outcome. Usually we keep them under hypothermia for 24 hours. Then comes the period of rewarming, which can be safely done by reducing the body temperature by 0.3 - 0.5 C /hr...and the aim is to normalise body temparature by 8 hours after starting to rewarm. Hemodynamic instability /electrolyte derangements/ arrhythmias can occur during this period...and should be addressed sooner than later.

Medications During Rewarming
Maintain sedation until a temperature of 35° C (95° F) is reached.
- If a neuromuscular blocking agent is infusing solely  to prevent shivering, discontinue the neuromuscular blocking agent before the sedative/analgesic agents.
- Do not discontinue the sedative/analgesic until the patient is moving or until the neuromuscular blocking agent has been discontinued for at least 3 to 5 half lives of the paralytic.


Hemodynamics
Monitor patient for hypotension. This is secondary to peripheral vasodilatation induced by rewarming. Gentle i.v fluids helps with this issue. Its physiologically reasonable ..not to use Ringer Lactate in this situation, as the hypothermic liver would not be able to metabolise lactate. Try to avoid vasopressors like dopamine during this period..due to the cardiac excitability from these drugs. Again ...physiologically phenylephrine would make more sense as it does not have a beta activity..and only has alpha atction.


Electrolytes
Discontinue potassium infusions during rewarming as potassium moves out of cells into the extracellular space.
Acetaminophen and external cooling p.r.n. to keep temperature less than 37.5° C (99.5° F) for 48 hours after  warming.