Written by Adam Blumenberg MD
Special Thanks to Sage Wiener MD
About halfway through your shift in the critical care area of the ED, you are wrapping up a conversation with the medical ICU team about an elderly patient in septic shock when you hear a shout for help from the triage area. You and your intern dash over where you find EMS pushing a stretcher into the resuscitation bay. On the stretcher sits a man. A sick man.
“I’ve been poisoned by my constituents!” he utters. He is bolt upright, eyes wide, skin sweaty & pale, and covered in blood from his chin down.
The telemetry monitor displays “TACHYCARDIA 113 — HYPOTENSION 76/30” in prophetic red letters.The EMT hands you the following rhythm strip:
The patient locks eyes on you...
You point to your intern and declare,
“Prepare for an intubation!” without missing a beat. “Put on your mask and gown while I activate the massive transfusion protocol and call the gastroenterologists for emergent endoscopy!”
Ten minutes later his airway is secure, and the third unit of warm packed red blood cells and second unit of fresh frozen plasma are infusing under pressure. You now perform your secondary survey which reveals the following:
Time to reassess
“Alright, he’s still tachycardic but no longer hypotensive. What are our critical actions?” you ask your intern, who responds “first and foremost we need source control. This is a massive upper GI bleed in the setting of liver failure. We need GI to control the bleeding, or he will die. Meanwhile, we need to continue the massive transfusion,” she says, rapping the fifth bag of PRBCs with her knuckle. “We should place a Blakemore, then start him on a proton pump inhibitor and an octreotide drip.”
“Not bad, not bad, but PPI and octreotide have not been proven effective. A medication that has been proven to save lives in esophageal variceal hemorrhage is … ”
“Ceftriaxone!” she exclaims.
“You got it!” you reply. “Excellent. Here is GI with their equipment.”
Controlling the source
As the gastroenterologists perform esophageal sclerotherapy and successfully control the hemorrhage, you leave the room to provide care for a patient with a subarachnoid hemorrhage and a patient with AIDS and a fever.
The triumphant gastroenterologist emerges from the resuscitation bay and demands a high five, proclaiming “I got all the bleeders! That dude is still hypotensive though, and it looks like he’s oozing from all four IV sites!”
“How could he be hypotensive? He’s not bleeding anymore and he’s received 10 units each of PRBCs, FFP, and platelets!” asks your intern.
“That’s a really good question. We need to reassess him. What could we be missing?” you reply, noting muscle fasciculation on his face and shoulder. “OK, go perform a RUSH exam, and let’s get a repeat EKG.”
As your intern views the ultrasound images she muses, “His heart is so hypokinetic. Plus it looks like he’s developing a coagulopathy even though we gave plenty of FFP and platelets. His ECG looks alright … except for this new QT prolongation. What did we give him that would prolong his QT?”
With those words the diagnosis dawns on you,
What’s In The Bag?
A unit of blood contains about 3 grams of citrate, which is added in order to chelate calcium and prevent stored blood from clotting. A healthy, well-perfused liver can clear 3 grams of citrate every 5 minutes. When there is liver dysfunction as in cirrhosis or frank hemorrhagic shock, the citrate clearance is reduced. The high citrate load may decrease the circulating ionized calcium. This can lead to the clinical effects of hypocalcemia, which include myocardial dysfunction, decreased vascular tone, QT prolongation, coagulopathy, muscle fasciculation, seizures, and of course, perioral paresthesias.
Acute hypocalcemia may additionally lead to metabolic alkalosis because the newly vacated albumin binding sites will sequester hydrogen ions. Metabolic alkalosis in a patient with anemia and shock can lead to grave consequences because alkalosis left-shifts the oxygen-hemoglobin dissociation curve leading to tissue hypoxia.
When hemoglobin binds oxygen tightly, there will be a deceptively high O2 saturation on the monitor.
Speaking of left shift…
PRBCs in storage contain 15% – 40% less of the chemical 2,3-BPG (2,3-bisphosphoglyceric acid) than circulating erythrocytes. This chemical right-shifts the oxygen-hemoglobin dissociation curve. What this translates to clinically is that transfused red cells are less effective than innate red cells at delivering oxygen to tissue.
One unit of blood product contains 250-300mL of colloidal fluid.
The INR of FFP is approximately 1.6.
10-20cc/kg of FFP must be given to raise the clotting factors by 20% (4-6 units in an adult).
Red blood cells
The hematocrit of PRBCs is 70-80%
pH 6.79 +/- 0.1
Bicarbonate 11.1 +/- 1.5 mmol/L
Potassium 20.5 +/- 7.8 mmol/L
Glucose 24.1 +/- 6.1 mmol/L
Lactic acid 9.4 +/- 4 mmol/L
Four units of blood deliver as much potassium as one 20mEq potassium rider.
Ca vs. Ca
Traditional teaching states that calcium gluconate requires metabolism by the liver to liberate the calcium ion, and is therefore less useful in shock states and liver disease. As a result calcium chloride is used during cardiac arrest, even though extravasation can cause significant tissue necrosis. Studies performed during the anhepatic phase of liver transplant showed no difference in rates of rise of serum Ca2+ levels between the two forms of calcium.
Take Home Points
– Transfused blood is inferior to innate blood at oxygen delivery to tissue.
– PRBCs contain high levels of potassium.
– Antibiotics directed against gram negative organisms have a survival benefit in patients with esophageal variceal hemorrhage.
Here is a photograph of Mycroft Voldemort Blumenberg. His hobbies including eating, sleeping, and homicide.
The author of a book in which characters learn about the world by watching their shadows had a mentor who died from poison. How does this poison work?
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