Grand Rounds Recap 6.17.20
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R4 capstone: respect your patients WITH Dr. gauger
How would you treat your patients if you saw them as a mother, father, brother, sister, niece instead of just a complaint? We can all do better at this.
Substance abuse is a large problem in the US. 5-10% of the population is affected by this.
15 million affected by alcohol , 2 million abuse opioids, 750,000 meth
1:8 ED visits are patients with substance abuse issues
We all have biases, but everyone deserves our respect. Don’t let your biases affect your empathy and care when taking care of your patients. Try to understand our patients as people.
We all decided we wanted to take care of the cold, hungry, unwashed. Try to understand our patients as people. We have the abilities to be leaders in this area for change.
Taming the sru WITH Dr. hall
Started with a tele call - Middle age female presenting with possible seizure? who was coming in unresponsive and hypoglycemic.
Vitals on arrival: Temp 86F, BP 70/36, HR 80, RR 22, O2 100%
Labs: VBG 6.81/24/4/-28.3, Lactate 20
Interventions: IVF, external warming, cultures, antibiotics. Bedside US showed collapsable IVC
Diagnosis: Thought to be severe alcoholic ketoacidosis with possible withdrawal seizure
Bicarb Administration in Severe Metabolic Acidosis
Controversial
RCT in 2018 showed no difference for 28-day mortality or organ failure after 7 days. However did show reduction in 28-day and need for dialysis in patients with severe kidney injury
Must reverse underlying cause
Consider in critically ill, pH < 7.1
Patient must have adequate ventilation prior to administration to avoid increased CO2, worsening overall acidemia
Alcoholic Ketoacidosis
Ketone bodies are fat-derived fuels, present in low insulin, high glucagon states
Malnourished alcoholics stop drinking and live in a low insulin state and start producing ketones.
Treatment includes dextrose containing fluids which stimulates insulin secretion. When stopping ketone production, will generate bicarb and correct acidosis
Must be careful of hypokalemia due to increased increased insulin secretion
Always consider thiamine administration as well
qikt: hepatic encephalopathy WITH dr. Leech and dr. Roblee
What is Hepatic Encephalopathy?
Brain dysfunction caused by liver insufficiency and/or portosystemic shunting, manifesting as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma.
Classifications:
Type A resulting from acute liver (not covered today)
Type B resulting predominantly from portosystemic bypass or shunting
Type C resulting from cirrhosis
Affects 30-45% of patients with cirrhosis
110,000 hospitalizations yearly in the USA
42% survival at 1 year after and episode of hepatic encephalopathy, goes down to 23% at 3 years
Pathophysiology
Byproducts of digestion in the gut produce ammonia, which is normally broken down into urea by the liver and excreted in the kidneys.
Clinical Presentation
Grade 0: minimal impairment, typically only noticed on formal cognitive testing
Grade 1 (covert): with trivial lack of awareness, inability to perform simple math, altered sleep rhythm, euphoria or anxiety
Grade 2 (overt): lethargy or apathy, obvious personality changes, inappropriate behavior, dyspraxia, ataxia, slurred speech, hyperreflexia
Grade 3 (overt): somnolence or stupor, disorientation to both time and space, confusion, bizarre behavior, clonus, rigidity, nystagmus, positive Babinski
Grade 4: coma (often no response to pain), opisthotonus
Workup
Question 1: Is hepatic encephalopathy the primary cause of altered mental status?
Consider your differential for AMS as HE is often a diagnosis of exclusion and we won’t know if that is the cause before the patient leaves the ED
A few to consider - Drug toxicity, EtOH withdrawal/intoxication, ICH, hypo/hyperglycemia, meningitis, Wernicke’s
Question 2: What has precipitated the HE?
Three most common causes include GI bleed, infection and dehydration
In 80-90% of cases a cause can be identified and treated
Other causes include: AKI/renal failure, electrolyte disturbance, constipation, medication nonadherence, change in dietary protein intake, changes in gut microbiome, large volume paracentesis
Consider these studies for workup
Labs: CBC, BMP, PT/INR, UDS, UA, ammonia*
*In an overtly encephalopathic patient, ammonia levels can be extremely variable and do not have any correlation with the patient’s mental status or grade of HE. Ammonia can also be falsely elevated in the case of difficult venipuncture, not placing the sample immediately on ice, or delayed time to analysis due to spontaneous release of ammonia by red blood cells in standing sample
Current guidelines suggest ordering an ammonia to help “think about a different diagnosis”. However, a negative ammonia doesn’t mean the patient doesn’t have HE, and a high ammonia doesn’t mean the patient has HE. It may be more helpful in acute encephalopathy rather than chronic patients
Imaging: CXR, CT head
Procedures: diagnostic paracentesis, rectal exam
Treatment
Lactulose: Traps ammonia in the gut, increases gut transit time (less absorption), promotes a favorable microbiome, decreases ammonia production
The 2014 AASLD (most recent guidelines) recommend
Lactulose as treatment of choice for overt HE
Lactulose for secondary prevention after an index event
DID NOT recommend routine treatment for minimal (covert) HE
DID NOT recommend primary prophylaxis for the prevention of HE except for patients at high risk.
However in 2016, Cochrane, provides support for primary prophylaxis in patients with cirrhosis to prevent HE.
Dosing: Titrate to 2-3 bowel movements per day. Start with 25mL of lactulose q1-2 hours with above goal.
There is poor compliance, lack of understanding, overuse
Rifaxamin: RNA polymerase inhibitor, decreases bacteria population, decreased ammonia production, reduces mucosal inflammation and visceral hypersensitivity
ISHEN 2020 guidelines: Rifaximin is an add on therapy to lactulose for prevention of HE recurrence after the 2nd episode or additional agent after 24 hours on lactulose with no response.
A recent (2013) randomized, controlled trial compared lactulose plus rifaximin to lactulose alone and found that more patients had complete resolution of hepatic encephalopathy than those treated with lactulose alone. These patients also had decreased mortality and hospital length of stay when compared with those on monotherapy.
