Emergency Medicine Posting 1

POST SPLENECTOMY SEPSIS
In 1952 King and Schumaker suggested that children who had undergone splenectomy were at risk for the development of bacterial infections, and the syndrome of overwhelming postsplenectomy sepsis (OPSS) was suggested by Diamond in 1969. The syndrome is unlike fulminating bacteremias and septicemia in individuals with normal splenic function. The onset is sudden, with nausea, vomiting, headache, and confusion leading to coma. The new infecting organism is a gram-positive organism in over half the cases, primarily Streptoccoccus pneumoniae. Blood cultures may occasionally demonstrate up to as many as 10 6 bacterial organisms per cu. mm. circulating in the bloodstream. Disseminated intravascular coagulation is common along with hypoglycemia, electrolyte imbalance, and shock unresponsive to antibiotics and fluid or pharmacologic support. Mortality has generally been reported as high as 50% and even up to 80% for pneumococcal infections. The true incidence of overwhelming postsplenectomy sepsis following a splenectomy from trauma is not well defined. Green and colleagues suggested that the risk of OPSS is 166 times the rate expected for the general population. Eraklis and Filler suggested that the incident rate of mortality from sepsis and OPSS is 78 times greater than that expected for the general population. Despite this increased frequency, overwhelming postsplenectomy sepsis remains a rare event. Singer's large review of 688 children who had undergone splenectomy for trauma demonstrated only a 1.45% incidence of postsplenectomy sepsis, but a 40% mortality. The occurrence of OPSS appears to be less following splenectomy for trauma when compared with splenectomy for congenital hematologic disorders. Nonetheless, the recognition of the severe nature of this entity has prompted many trauma surgeons to more aggressively attempt splenic salvage. Animal laboratory evidence suggests that at least 50% of the splenic tissue mass must be preserved to prevent overwhelming postsplenectomy sepsis. The immunologic function of the spleen that appears to be most beneficial in preventing OPSS is the spleen's capacity for clearance of blood-borne particles and the provision of circulating opsins, which assist in cell-mediated immunologic functions

Ventricular interdependence is the term used to describe the dysfunction of one ventricle secondary to a disorder of the other, mainly due to the involvement of the interventricular septum which is common to both ventricles. During spontaneous inspiration, right ventricular volume increases, pushing the interventricular septum towards the left ventricle. This leads to an increase in left ventricular filling pressure with an unchanged or lower left ventricular end diastolic volume. This is a diastolic interventricular interaction which is always present [1].

Studies have shown that twenty to forty percent of right ventricular output and systolic pressure generation are contributed by left ventricular contraction [2].

Right ventricular diastolic dysfunction can be associated with left ventricular dysfunction even in the absence of pulmonary hypertension or direct involvement of the right ventricle by the same disease process as coronary artery disease. Similarly pressure or volume overload of the right ventricle can affect the systolic or diastolic function of the left ventricle due to the effect on the interventricular septum. This has been documented in certain cases of chronic obstructive pulmonary disease, pulmonary hypertension and atrial septal defect.

The effect of ventricular interdependence is also striking in cardiac tamponade when the filling of the ventricles is limited by a fixed total pericardial space. Dornhorst’s theory states that inspiratory filling of the right ventricle causes collapse the left ventricle in this situation, reducing left ventricular output and explains the pulsus paradoxus in cardiac tamponade [5]ricular Interdependence and pulsus paradoxus in cardiac tamponade

ABG IN ASTHMA
In severe asthma, the normal expectation is respiratory acidosis.
However the VBG of a child with severe asthma is shown below:
ph – 7.31
PaCO2 – 34.7
HCO3 – 17.4
paO2 – 34.9
BE - -7.4
Interpretation ; Based on the results, the pH is low (acidosis), the PaCO2 is low (alkalotic) and the bicarbonate is low (acidotic). Hence this is metabolic acidosis partially compensated by respiratory alkalosis. The base excess further supports the underlying metabolic acidosis.
The partial pressure of oxygen is low, indicative of impending type 1 respiratory failure.

Explanation for metabolic acidosis:
The causes of metabolic acidosis in asthma are increased lactic acid production by respiratory muscles due to prolonged and increased work of breathing, tissue hypoxia secondary to reduced cardiac output and ventilation-perfusion mismatch, decreased lactate clearance due to hypoperfusion of the liver, and excessive renal bicarbonate loss due to compensation for a preceding period of hypocapnia and respiratory alkalosis

How Beta Blockers may lead to Hyperkalemia:
1. Beta blockers suppress catecholamine-stimulated renin release, thereby decreasing aldosterone synthesis.
2. More importantly nonselective beta blockers decrease cellular uptake of potassium

During treatment of hyponatremia, the serum sodium (salt level in the blood) is not allowed to rise by more than 8 mmol/L over 24 hours.

Magnesium has a clear role in the emergency management of a number of conditions.

It should be used as first line therapy in eclampsia and torsade de pointes ventricular tachycardia.

It has a clearly defined role as a second line therapy in acute severe bronchial asthma.

Hypomagnesaemia should be considered in patients with biventricular failure presenting with malignant arrhythmias.

Magnesium should be considered as a temporising measure in cases of severe digoxin toxicity while using Fab antibodies as the specific antidote.

Magnesium is safe and easy to use.

In marked hyperglycemia, ECF osmolality rises and exceeds that of ICF, since glucose penetrates cell membranes slowly in the absence of insulin, resulting in movement of water out of cells into the ECF. Serum Na concentration falls in proportion to the dilution of the ECF, declining 1.6 mEq/ L for every 100 mg/dL (5.55 mmol/L) increment in the plasma glucose level above normal. This condition has been called translational hyponatremia because no net change in total body water (TBW) has occurred. No specific therapy is indicated, because Na concentration will return to normal once the plasma glucose concentration is lowered.
SERUM SODIUM CORRECTION IN HYPERGLYCAEMIA:
Corrected Sodium
= Measured sodium + (((Serum glucose - 100)/100) x 1.6)

PREGNANCY AND CPR:
The 2015 American Heart Association guideline on cardiac arrest in pregnancy recommends the same hand position for chest compressions in pregnant women and nonpregnant adults. Previous guidelines suggested a more cephalad hand position in pregnancy to adjust for elevation of the diaphragm by the gravid uterus; however, a recent imaging study showed no significant vertical displacement of the heart in the third trimester relative to the nonpregnant state.

1. The recommended chest compression rate is 100-120 per minute which is updated from the at least 100/min.


2. The recommended chest compression depth is 5-6 cm or just over 2 inches, but not more than 6 cm as too deep can be harmful.


3.Use Audiovisual devices such as metronomes and compression depth analyzers which can be used to optimize CPR quality.


4. The routine use of impedence threshold devices (ITDs) alone or mechanical chest compression devices alone are not recommended, however in out of hospital situations where manual compressions are difficult due to physical space limitations, mechanical devices may be useful.



5.ECMO or ECPR may be considered for selected patients with refractory cardiac arrest where a reversible cause of cardiac arrest is suspected.


6. Vasopressin has been removed from the algorithm altogether, and an emphasis on EARLY administration of epinephrine is stressed.


7. Ultrasound has been added as an additional method for helping to confirm ROSC and for confirming ETT placement.


8. Use maximum inspired oxygen during CPR and then after ROSC, titrate oxygen to an oxygen saturation of 94% rather than continuing maximum oxygen delivery.


9. A low end tidal CO2 in intubated patients after 20 minutes of CPR is associated with a very low likelihood of survival, and this factor should be used in combination with other factors to help determine when to terminate resuscitation.


Emergency PCI is recommended for all patients with STEMI AND for hemodynamically or electrically unstable patients without ST elevation for whom a cardiovascular lesion is suspected.


ACLS GUIDELINES 2015

Here is the new BLS guideline from AHA for 2015.
It basically says push harder and faster.

eccguidelines.heart.org