–simple pancreatitis presents with fever ~70% of the time (does NOT mean it’s infected)
-use BISAP score to risk stratify (predicts mortality in ED)
-hyperTG is not that uncommon => when diagnose, send lipid panel
-diagnosed by CT (emulsified, infected pancreatic tissue, often gas/emphesematous changes)
-ONLY time you give abx in pancreatitis per EBM
-give carbipenams (meropenam) + flagyl for best penetration into pancreatic tissue
-get tylenol level (and salicylate) in jaundiced pt
Vomiting or altered/drowsy: evaluate for shunt malfunction
-look for hydrocephalus
—get rapid sequence MRI instead of CT head (these pts get many, many CTs)
—either may require sedation (etomidate)
-look for kinks in the shunt
—-shunt series (skull xray, cxr, kub)
Fever + irritability: consider shunt infection
-erythema of skin overlying hardware
-other causes: ears, throat, lungs, abd
-labs, blood culture, UA and culture +/- rapid strep and culture
1. Does the shunt need to be tapped?
2. Call NSG (at MMC) vs do it yourself?
-alpha & beta effects (inotropy, chronotropy)
-one ampule = 10 mL syringe = contains 1mg total
-thus 1mg / 10 mL = 1000 mcg / 10 mL ==> 100 mcg / 1mL
Push Dose Epi
-never give cardiac doses (1mg) to pt with a pulse
-use a 10mL saline flush: waste 1mL, draw up 1mL epi (contains 100 mcg) from cardiac ampule
-you now have 100 mcg / 10 mL = 10 mcg per mL in this flush
Dirty Epi Drip
-take the entire ampule (10mL syringe) of cardiac epi and inject into 1L NS bag
-you’ve put 1mg epi into 1000mL NS = 1000 mcg / 1000 mL = 1mcg/mL epi drip
-run wide open in anaphylaxis
-pure alpha, so all inotropy and no chronotropy
-3 components: Diabetes (BG >250), Ketones (serum/urine BHB*, acetone, acetoacetate), Acidosis (pH<7.3, bicarb <18)
(1) Fluid resuscitate: 15-20 cc/kg NS bolus within first hour
(2) Supplement K if <4 (No benefit for supplementing phosphate)
(3) Give insulin regular/Humalog 0.1 U/kg gtt
Continue until Anion Gap closes. Repeat blood gases q1h.
If glucose drops <150, start D5 0.45NS alongside insulin.
Evaluate for precipitants.
-Note: it is possible for the anion gap to be low/closed at diagnosis/???
-Note: if acidosis is worsening, look for concomitant hyperchloremic metabolic acidosis
*BHB is most sensitive. (BHB comprises ~78%. Acetoacetate ~20%, but is unstable and breaks down into CO2 and acetone, which comprises the remaining 2%.)
Euglycemic DKA = metabolic derangement (low insulin / high glucagon) causing excess ketone production without hyperglycemia
– vomiting is most common symptom
– look for elevated AG and acidosis without high BGM – send urine and serum ketones!
– still require iv hydration and lyte replacement
– require iv insulin to close the gap – however will need to start D5-containing fluids concomitantly
– associated with sodium-glucose co-transporter 2 inhibitors (SGLT-2 inhibitors, or the “zins”)
-Glucose usually very high (600-1000), no/minimal ketones, pH>7.3
-HONK is managed the same way, except the fluid deficit is much greater (the dehydration is chronic). No established guidelines.
-CXR not sensitive – minimum 200-250cc (large) pericardial fluid produces cardiomegaly
-TEMPORIZE by pushing fluids to increase preload and Trendelenburg
-APPROACHES include subX vs parasternal: choose based on whichever view you see the largest pocket of fluid
-may use central line kit
-Place needle just inferior and lateral to the right of the subX process. Aim at pt’s left shoulder. Numb the tract. Try to visualize needle on US but if pt is in extremis, it’s ok not to (basically blind procedure) as long as you advance cautiously. Take off as much fluid as you can.
-GOAL: Take off enough fluid to stabilize the patient. If tamponade recurs, repeat pericardiocentesis and consider placing a catheter/drain (Rosen’s)
-COMPLICATIONS: myocardial perforation, pneumothorax, laceration of LIMA (esp parasternal approach) or coronaries, dysrhythmias, liver lac (expected as part of subX approach)
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