Our esteemed doctors Madhavan and Garcia presented a fascinating two-part case from Monday and today. Our patient is a young man with a history of heavy alcohol use who presented with diffuse abdominal pain, nausea, and nonbloody nonbilious emesis.
He was febrile and tachycardic on exam, but otherwise stable. His abdomen was diffusely tender to palpation and his bowel sounds were hypoactive. His lipase was 563 and a CT of his abdomen and pelvis show fat stranding around his pancreas with a pseudocyst near the pancreatic head.
What are the criteria to diagnose acute pancreatitis?
You must fulfill at least 2 out of the following 3 criteria:
- Characteristic pain (acute onset and severe epigastric pain +/- radiation to the back)
- Lipase 3x the upper limit of normal or higher
- Evidence of pancreatitis on imaging (contrast-enhanced CT abdomen is the modality of choice if the patient can tolerate the contrast load)
Our patient met 2-3 of these. Because his pain was not necessarily characteristic given its diffuse nature, a CT A/P was ordered. If the ER physician had considered him to have pain characteristic of acute pancreatitis, he would not need imaging to make the diagnosis. However, it is wise to get an abdominal ultrasound for patients with their first episode of pancreatitis to rule out gallstone pancreatitis even if there is a history of alcohol use.
Why did this patient get acute pancreatitis?
The most likely etiology in this case was alcohol use, which is the most common cause of acute pancreatitis in the United States. Other possible etiologies include:
Hypertriglyceridemia or hypercalcemia
What special findings can be seen in the physical exam of a patient with acute pancreatitis?
Physical exam findings of patients with acute pancreatitis should include epigastric tenderness to palpation and may include decreased lung sounds at the lung bases, abdominal distension, decreased bowel sounds. Grey-Turner and Cullen’s signs are ecchymosis at the flanks or umbilicus respectively. These are rare and if present, should prompt consideration of retroperitoneal bleeding from pancreatic erosion into adjactent vascular structures. Panniculitis is an uncommon finding associated with acute pancreatitis that presents as inflamed, erythematous, painful nodules on the lower extremities due to fat necrosis from circulating pancreatic enzymes.
Treatment of acute pancreatitis consists of:
- Aggressive fluid resuscitation
- Pain control (opting for IV opiates via PCA is justified)
- Nutrition: As soon as the patient can tolerate PO, they should be fed even in the setting of ileus. If the patient is unable to take PO, NJ tube should be inserted and nutrition begun within 3-4 days.
What does the pseudocyst on this patient’s CT scan tell you about the course of his disease?
He has most likely had an episode of pancreatitis in the past because pseudocysts to not develop acutely. They are seen 4 weeks after an episode of acute pancreatitis.
What are the complications of acute pancreatitis?
Local complications include fluid collection, walled off necrosis, acute necrotic collections, pseudocyst formation, and hemorrhage from invasion of adjacent vascular structures. These patients can also get ARDS, abdominal compartment syndrome, small bowel obstruction or ileus, pleural effusions, pancreatic ascites, splenic vein thrombosis, and chronic pancreatitis. Pseudoaneurysms can also be formed, which is when a vessel gets eroded and begins to drain blood into a pseudocyst, which becomes a pulsating hematoma.
In the ED, our patient received 3L NS and was placed on an LR infusion at 175 cc/h. Over the following hours, he became acutely hypoxic and required intubation and mechanical ventilation. CXR showed diffuse pulmonary infiltrates with an ABG of 7.42/39/111 on a PEEP of 5 and FiO2 of 100%. His echocardiogram was normal and he didn’t have elevated JVP or peripheral edema.
What are the criteria to diagnose ARDS?
We diagnose ARDS with the Berlin criteria, which have thee components and are as follows:
- Timing (within 1 week of known clinical insult or respiratory symptoms)
- Imaging with bilateral opacities not completely explained by effusions, lobar/lung collapse, nodules, or cardiogenic pulmonary edema. This requires objective assessment such as TTE to exclude cardiogenic edema.
- Hypoxia: We use the PaO2/FiO2 ratio (PF ratio) to evaluate hypoxia (200-300 mild, 100-200 moderate, <100 severe)
What is happening pathophysiologically in ARDS?
Inflammatory cytokines and cells are causing diffuse alveolar damage. This impairs gas exchange, causes alveolar collapse, and decreases surfactant functioning.
What should be your overall ventilation strategy for this patient?
Low tidal volume, which necessitates a high respiratory rate to maintain minute volume.
Higher PEEP to stabilize alveoli and increase recruitment.
Although a higher FiO2 is required to oxygenate these patients, minimizing FiO2 as much as possible to prevent oxidative damage is important.
How should you calculate the patient’s initial tidal volume?
First, you will need their predicted body weight, which can be calculated via formulas or MD calc or looked up based on their height. Keep in mind that there are different formulas and tables for men and women.
Men: 50 + 2.3[(height in inches)-60]
Women: 45.5 + 2.3 [(height in inches) -60]
Tidal volumes for ARDS patients should be low, start at 6mL/kg.
How should you set their initial respiratory rate?
Your goal is to maintain the patient’s baseline minute ventilation despite having to use a decreased tidal volume to protect their damaged lungs.
Minute ventilation = tidal volume x respiratory rate
Your respiratory rate should never go above 35 and you should watch to make sure your patient is not breath stacking/auto-PEEP.
How do you set your PEEP and FiO2?
Start with a PEEP of 5 and an FiO2 of 100%. Over the next hour, you should wean FiO2 to as low as possible while adjusting PEEP using the ARDS Network guidelines, which includes a chart of appropriate PEEP levels per FiO2. Always start at the lowest PEEP included if there is a range. You want the lowest FiO2 possible to maintain an oxygen saturation by pulse oximeter of 88-95% OR PaO2 on ABG 55-80mmHg.
How do you make sure your pulmonary pressures are not too high?
Monitor plateau pressure Q4 hours and every time you make adjustments to ventilator settings. Plateau pressures should be maintained below 30 for ARDS patients. If your plateau pressure is too high, you have three main options:
- Decrease your tidal volume (this will require increasing your respiratory rate to maintain minute ventilation)
- Decrease your PEEP (this may decrease recruitment and cause hypoxia)
- If present, treat any ventilator dyssynchrony with neuromuscular blockade
What about the pCO2?
The main problem in ARDS is hypoxia, but when we are using a low tidal volume ventilator strategy, it is easy to make our patients hypecapneic. Some patients are so difficult to ventilate due to their low lung compliance that it is impossible to maintain normal oxygen and carbon dioxide without exceeding your plateau pressure limit of 30. For this reason, a strategy of permissive hypercapnea is employed in ARDS.
A pH 7.25-7.5 is tolerated in these patients without an increase in mortality.