Episode 8 – Acid-Base and Hyponatremia

Episode 8 (iTunes or Listen Here)

The Free Open Access Medical education (FOAM)

This week we review Dr. David Story’s talk from SMACC GOLD, “Is Chloride a Poison?”  Dr. Story discusses the Stewart ion approach to acid-base, driven by the independent variable, the Strong Ion Difference (SID), which is the difference between the sums of concentrations of the strong cations and strong ions (typically Sodium and Chloride). He also reviews literature that suggests that there may be morbidity and even mortality associated with large volume infusions of 0.9% NaCl (NS), although more research is required in this arena to determine the patient oriented sequelae. Perhaps we should be using more balanced solutions such as lactated ringers (LR).

Also, SMACC  is awesome, listen to the talks from SMACC GOLD and come meet us in Chicago next June!

Literature on the topic:

Other FOAM Acid-Base Resources:

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapters 19,21; Rosen’s (3e) Chapters 124, 125 …but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

IV Fluids – Know the Composition (PV card from ALiEM)

Red - Too Much, Yellow - Too Little, Green - Just Right
Red – Too Much, Yellow – Too Little, Green – Just Right

Costs – NS (0.9%) is the cheapest, coming in at just over a US dollar per Liter and LR is slightly more expensive (most estimates are approximately $0.50 more per liter).  Plasma-lyte is more expensive, costing several dollars more per liter.

Downsides of Normal Saline (NS, 0.9%)

  • Hypertonic, hypernatremic, hyperchloremic – it has a little too much of everything and is acidic, with a pH of 5.0 [1]
  • The SID (Strong Ion Difference) of NS is 0, far less than the physiologic or normal SID of 38.  This is where the non-anion gap acidosis comes into play [1].

Caution with Lactated Ringers (LR)

  • LR contains calcium and some labs studies have shown that this may cause clotting; thus, major societies say LR is incompatible with blood products.  There are some studies to show that this may not be as big of a deal as previously thought: Albert et alCull et alLorenzo et al.
  • May interfere with Lactate clearance -A study of healthy individuals demonstrated that LR did not affect serum lactate levels [2].  However, often we are doing these large volume resuscitations in the critically ill who may have hepatic insufficiency and, thereby, reduced lactate clearance.  There is worry that LR may increase the serum lactate, making it difficult to gauge resuscitation by lactate clearance.  Paul Marino’s ICU Book states that significant skewing of the lactate is unlikely unless the patient’s ability to hepatically clear lactate is nil and the patient has gotten several liters of LR [1].

FOAM Resources:

Hyponatremia  – Na+ <135 mEq/L

Symptoms: often asymptomatic but may see vague symptoms such as nausea, vomiting, myalgias, lethargy.  Values <120 mEq  more associated with symptoms and <113 mEq, may see seizures/coma.

Causes:

  • Hypovolemic – Extra-renal: dehydration (vomiting, diarrhea, small bowel obstruction, burns), infusion of hypotonic fluids, Renal: thiazide diuretics, Renal Tubular Acidosis, osmotic diuresis, aldosterone/mineralocorticoid deficiency
  • Euvolemic – SIADH (syndrome of inappropriate secretion of antidiuretic hormone), water intoxication, drugs (NSAIDs, APAP, TCAs, sulfonylureas, morphine, carbamazepine, etc), beer potomania
  • Hypervolemic – think organ failure and people who are third spacing fluids. Congestive Heart Failure, Liver Failure, Renal Failure

Other FOAM Hyponatremia Resources:

Generously donated Rosh Review questions (scroll for answers)

Question 1.[polldaddy poll=8191357]

Question 2. A 23-year-old woman presents with seizures. The patient received 2 mg of lorazepam by EMS but continues to seize. Serum lab tests show the following: sodium 118, potassium 3.6, chloride 90, bicarbonate 21, BUN/Cr 10/1.0, glucose 89. [polldaddy poll=8191360]

Additional References:

1.Tizard, H.  Chapter 12: Colloid and Crystalloid Resuscitation.  Marino’s The ICU Book, ed 4.Lippincott Williams & Wilkins, 2007.

2.Didwania A, Miller J, Kassel D, Jet al. Effect of intravenous lactated Ringer’s solution infusion on the circulating lactate concentration: Part 3. Results of a prospective, randomized, double-blind, placebo-controlled trial.Crit Care Med. 1997 Nov;25(11):1851-4.

Answers.

1.C -The syndrome of inappropriate secretion of ADH (SIADH) is defined by the secretion of ADH in the absence of an appropriate physiologic stimulus. Its hallmark is an inappropriately concentrated urine, despite the presence of a low serum osmolality and a normal circulating blood volume. Causes of SIADH include central nervous system disorders, pulmonary disease, drugs, stress, pain, and surgery. Therefore, the above patient, with a known history of lung cancer and hyponatremia, most likely has SIADH and exhibits the following lab findings: serum osmolarity low, urine osmolarity high, urine sodium high. Psychogenic polydipsia (D) is a rare cause of euvolemic hyponatremia and is seen in psychiatric patients who consume large amounts of free water (in excess of 1 L/hr). This large consumption overwhelms the kidney’s ability to excrete free water. Patients will exhibit serum osmolarity low, urine osmolarity low, urine sodium low. Diabetes insipidus (B) results in the loss of large amounts of dilute urine from the loss of concentrating ability in the distal nephron. This may be due to a central cause—such as the lack of ADH secretion from the pituitary—or a nephrogenic cause—such as the lack of responsiveness to circulating ADH. Laboratory workup that invariably shows serum osmolarity high, urine osmolarity high, urine sodium low (A) rarely occurs.

2.A-This patient presents with prolonged seizure activity and hyponatremia and should emergently be treated withhypertonic saline. Hyponatremia is defined as a serum sodium level <135 mEq/L and is the second most common electrolyte abnormality after hypokalemia. The symptoms and signs of hyponatremia depend on the patient’s volume status, the cause and the rapidity of the change in serum sodium. Typically, patients with acute changes will have more severe symptoms including nausea, vomiting, confusion, stupor and seizures. Chronic hyponatremia will typically present with mild neurologic symptoms as well as lower serum sodium levels than acute hyponatremia. In patients without neurologic symptoms, volume status should be assessed and additional labs should be sent off to determine the cause of hyponatremia (urine sodium, osmolarity etc.). Patients with neurologic symptoms should be aggressively treated with 3% hypertonic saline. When correcting serum sodium, it is important to increase the serum sodium by no more than 0.5 mEq/L/hour and by no more than 10 – 12 mEq/day. More rapid changes can lead to central pontine myelinolysis, a crippling neurologic disease.

Episode 6 – Hepatic Emergencies

Episode 6 – Liver Emergencies (iTunes or Listen Here

This episode is a response to Dr. Nick Genes tweet:

 Here’s the slideset he posted, filled with excellent pearls.

The Free Open Access Medical Education (FOAM)

We review a post from the Maryland Critical Care Project entitled  Chyle- coming to a paracentesis near you! The post reviews the etiology, epidemiology, and treatment for the rare but morbid chylous ascites.

For more excellent FOAM on liver emergencies:

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapter 83; Rosen’s (8e) Chapter 90 …but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Spontaneous Bacterial Peritonitis

  • Diagnosis – paracentesis results revealing >1000 WBCs or >250 polymorphonuclear neutrophils (PMNs). Many patients lack abdominal pain or clear symptoms.  If a patient is sick and the benefit of identifying a source is likely to outweigh the benefit.
    • ACEP cites a relative contraindication of INR >2 [3]. Yet, the AASLD recommends that “coagulopathy should preclude paracentesis only when there is clinically evident hyperfibrinolysis (three-dimensional ecchymosis/hematoma) or clinically evident disseminated intravascular coagulation” [4].
    • Rosen’s supports giving blood products to reverse “significant coagulopathy” prior to paracentesis but note that the AASLD also does NOT support giving blood products to reverse coagulopathy prior to paracentesis, stating that “these patients regularly have normal global coagulation because of a balanced deficiency of procoagulants and anticoagulants[4].
  • Treatment – Third generation cephalosporin
  • Prevention – some patients are on prophylaxis for SBP (often norfloxacin or TMP-SMX).  In cirrhotic patients with upper gastrointestinal bleeds, some have found a number needed to treat (NNT) of 22 for mortality although only one study was placebo controlled.

Hepatic Encephalopathy (Calculator) – graded I-IV.  Remember, Grade II = asterixis, Grade IV is coma.

  • Diagnosis of exclusion – a high ammonia does not mean the patient has hepatic encephalopathy as the cause of their symptoms.
  • Check for precipitants – WikEM has a good list but it includes things like gastrointestinal bleed, electrolyte abnormalities (hyponatremia, hypokalemia), infection, drugs, etc.
  • Ammonia level does not correlate with degree or grade of encephalopathy.

Hepatotoxic Drugs – check out the tables in Rosen’s/Tintinalli.  The NIH website Liver Tox, is also quite helpful. A few highlights

  • Acetaminophen – we don’t cover this but it’s something that everyone needs to know (WikEM, Life in the Fast Lane).
  • Amoxicillin-clavulanate (mixed cholestatic and hepatocellular toxin, theorized to be mostly http://www.mindanews.com/buy-effexor/ from the clavulanate) – per the NIH “currently the most common cause of drug induced liver disease in most large case series from the United States and Europe.”
  • Amiodarone, Buproprion
  • Cholestatic examples include haloperidol, verapamil, carbemazepine

MELD score – Quantifies end-stage liver disease for transplant planning

Generously donated Rosh Review questions (scroll for answers)

Question 1. A 54-year-old man is brought into the ED for altered mental status. He is markedly disoriented with confused speech and is unable to follow any commands. A musty odor is noticed when he breathes. Medical history is positive for IV drug abuse. [polldaddy poll=8141043]

Question 2. A 25-year-old previously healthy man presents to the ED with abdominal pain, weakness, confusion, and yellow discoloration of his skin. Laboratory studies reveal markedly elevated AST, ALT, total bilirubin, and serum creatinine. Review of his records shows that he was seen and discharged from the ED 3 days ago for vomiting, abdominal cramps, and watery diarrhea that he developed after a day of hiking in the woods. [polldaddy poll=8141059]

References:

1.O’Mara SR, Gebreyes K.  Chapter 83. Hpeatic Disorders, Jaundice, and Hepatic Failure. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011. p 566-574

2. Oyama L.  Chapter 90.  Diseases of the Liver and Biliary Tract .  Rosen’s Emergency Medicine, 8e.  2014.  p 1186-1204

3. Scheer D, Secko M, Mehta N.  Focus On: Ultrasound-Guided Paracentesis. November 1, 2012.

4. 3.  Runyon BA.  Management of Adult Patients with Ascites  Due to Cirrhosis: Update 2012.  (2013) doi: 10.1002/hep.00000

Answers.

1.  C – Grade I (A) is characterized by disordered sleep, irritability, depression, and mild cognitive dysfunction. Grade II (B) is characterized by lethargy, disorientation, confusion, personality changes, and asterixis. Grade IV (D) is characterized by coma.
2.B – Mushroom toxicity can be divided into 2 groups based on the onset symptoms: early onset toxicity and delayed onset toxicity. Symptom onset 0–4 hours after mushroom ingestion typically indicates a benign course, whereas delayed symptom onset (6–24 hours) is a marker for ingestion of mushrooms with potential for serious toxicity. The patient in the clinical scenario most likely ingested Amanita phalloides, aka the death cap mushroom, while on his hiking trip. This mushroom contains amatoxin, which causes fulminant hepatic failure over a course of days. Amatoxins are responsible for more than 90% of mushroom deaths worldwide. The classic presentation of amatoxin poisoning occurs in 3 phases: (1) delayed GI toxicity (abdominal cramping and diarrhea) 6–24 hours after ingestion; (2) a period of false recovery when the patient appears improved but liver enzymes rise; and (3) the final phase of markedly elevated transaminases, hyperbilirubinemia, DIC, and multiorgan failure 2–4 days after ingestion. Renal failure is also a hallmark. No antidote exists for amatoxin toxicity, and treatment involves supportive care. GI decontamination by activated charcoal may be of benefit, but hemodialysis is not effective.

 

Episode 4 – Transfusions and Ingested Foreign Bodies

Episode 4 – Transfusion Emergencies (iTunes or Listen Here

The Free Open Access Medical Education (FOAM) –from Dr. Ryan Radecki’s erudite blog, Emergency Medicine Literature of Note..

Infections & Transfusions” – a JAMA meta-analysis found that higher hemoglobin targets were associated with an increased incidence of infection with a number needed to harm of 20-38.  The  group with a target level of 7-9 g/dL had an infection rate of 11.8% (95% CI, 7.0%-16.7%)  compared with an infectious complication rate of 16.9% (95% CI, 8.9%-25.4%) in the “liberally” transfused group.

Grilling Injuries on Memorial Day” – Grilling isn’t risk free.  Dr. Radecki reviewed a case series of six individuals who presented in one year to a hospital after ingesting meat cooked on a grill.  Three patients had neck pain with wire grill bristles removed via laryngoscopy and three had abdominal pain necessitating removal – 2 by colonoscopy and 1 with urgent surgery secondary to intestinal perforation.

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapters 233; Rosen’s (8e) Chapter 7…but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Transfusion Reactions

Immediate Reactions – great FOAM summary from Life in the Fast Lane: Transfusion Risks, Transfusion Reactions 

Screen Shot 2014-06-08 at 9.39.12 PM

 

 

 

 

 

 

 

The Ones Our Patients Care About (Infectious – statistics are US based)

  • Bacterial contamination is rare: 1/500,000 – 1/1,000,000
    • Most common pathogen: Yersinia Entercolitica
  • More common in platelets: 1/1000-1/2000 per Rosen, CDC, and the AABB  (Tintinalli cites 1 in 6 million)
  • Most Common virus: Parvovirus B19 (1 in 10,000).  The others are very very rare: HIV and Hepatitis C > 1 in 1 million, Hepatitis B 1 in 100,000-200,000

Ingested Foreign Bodies

  • Beware the button battery. These can cause necrosis within hours in the esophagus and must be removed ASAP.
  • Objects that are irregular, very sharp, or have dimensions greater than 2.5cm in width or 6 cm in length that are still in the stomach or duodenum – call GI to have these removed via endoscopy.

Generously donated Rosh Review questions (scroll for answers)

Question 1 A 55-year-old woman is receiving a blood transfusion due to persistent vaginal bleeding and a hemoglobin of 5 mg/dL. While receiving the transfusion, she develops fever, chills, back pain, pain at the site of transfusion, and tachycardia. [polldaddy poll=8109900]

Question 2 A 28-year-old man presents with a 1-day history of rectal bleeding. In the ED, he is hypotensive, thrombocytopenic, and is found to be passing melena. He receives a transfusion of platelets and packed red blood cells as part of his resuscitation. Twenty minutes after the start of his platelet transfusion, his BP is 90 mm Hg systolic, he becomes dyspneic, and his oxygen saturation drops from 99% on room air to 91% on 2L of oxygen supplementation. On exam, you note rales at the lung apices and that he is using accessory muscles to breathe. His chest radiograph shows diffuse interstitial infiltrates. [polldaddy poll=8109907]

Question 3 [polldaddy poll=8109908]

 

References:

Emery M.  Blood and Blood Products.  Rosen’s Emergency Medicine. 2014: 8th ed. p 75-80.e2

Coil CJ, Santen SA.  Transfusion Therapy  Tintinalli’s Emergency Medicine: A Comprehensive Review. 7th ed.

Hillyer CD, Josephson CD, Blajchman MA, et al. Bacterial contamination of blood components: risks, strategies, and regulation: joint ASH and AABB educational session in transfusion medicine. Hematology Am Soc Hematol Educ Program. 2003:575-89.

1. C – Up to 20% of all transfusions may lead to some type of adverse reaction. Although most of these reactions are minor, some are life-threatening. The patient is having an acute intravascular hemolytic reaction. This occurs when the recipient’s antibodies recognize and induce hemolysis of the donor’s red blood cells and may result in activation of the coagulation system and disseminated intravascular coagulation. This type of reaction typically presents with back pain, pain at the site of transfusion,headache, fever, hypotension, dyspnea, tachycardia, chills, bronchospasm, pulmonary edema, bleeding, and development of renal failure. First, stop the transfusion. Then initiate intravenous hydration to maintain diuresis.

2.D- This patient is most likely suffering from transfusion-related acute lung injury (TRALI), one of the leading causes of transfusion-related mortality. It is most closely associated with platelet and fresh frozen plasma transfusions, though cases have been reported with packed red blood cells since there is some residual plasma in the packed cells. Symptoms begin abruptly during transfusion or within 6 hours and resemble adult respiratory distress syndrome with noncardiogenic pulmonary edema, dyspnea, hypoxemia, and bilateral infiltrates on chest radiograph.

3. A- The patient is experiencing an allergic reaction without serious signs or symptoms. The transfusion does not need to be stopped for such a reaction; an antihistamine will help to relieve symptoms.

Episode 3 – Ear Emergencies

Episode 3 – Ear Emergencies (iTunes

The Free Open Access Medical Education (FOAM) – SMART EM Pseudoaxioms 2 and Literature Update

The podcast reviews:

  • Bullous Myringitis, a painful infection of the tympanic membrane, is typically caused by viruses, strep. pneumoniae and moraxella and, less commonly, mycoplasma.  The boards have caught up with this. Check out this review by Mellick.
  • PHANTOM-S trial: Use of the STEMO (Stroke Emergency Mobile – an ambulance with neurologist and a CT scanner for suspected strokes) reduced mean alarm-to-treatment time by 25 minutes (95% CI, 20-29; P < .001) without an appreciable neurologic benefit for this intensive intervention.
  • An article by Gregg et al in the NEJM discussed incredible improvements in diabetes outcomes as a result of tight glycemic control. Dr. Newman asserts that much of this is secondary to dilution, as the definition of diabetes changed in 1997.  This resulted in more people with less severe disease being diagnosed with diabetes.

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapters 237; Rosen’s (8e) Chapter 92.  A good read on common ear emergencies from EBMedicine…but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Bullous Myringitis

This is a painful infection characterized by bullae on the tympanic membrane (TM), which has a richly innervated outer epithelium (hence the severe otalgia). Patients may collect fluid behind their TM or have a concomitant otitis media.

Etiology: viruses, typical otitis media pathogens.  Mycoplasma and chlamydia have been associated with bullous myringitis but the association is unclear and these are not the most common causes.

Treatment: pain control, pain control, pain control.  Antibiotics are optional in most cases. But then again, antibiotics are not necessary in most cases of otitis media.  Both Rosen and Tintinalli are on board with this.

Perforated Tympanic Membrane

Photo:Didier Descouens (Wikimedia Commons)

Etiology: infection, trauma (q-tips, instrumentation), changes in pressure (diving, flying)

Treatment:  Keep the ear canal dry, follow up with ENT.  Most of these patients can go home.  If the injury is in the posteriorsuperior aspect of the TM or secondary to penetrating trauma, they should see ENT within 24 hours because they may have damage to the bones of the middle ear.

Auricular Hematoma

Etiology: Blunt trauma (often associated with boxing, fights, or termed “rugby ear“)

Treatment:  Incision, drainage, and compression dressing/splint.  Photo guide to repair.

Ototoxic Agents (great table in Tintialli 8 e, Ch 237, p1551)

Risk of hearing loss typically increases with exposure to medication (dose and length of use) and issues with clearance such as renal insufficiency may cause medications to hang around longer than anticipated or at higher levels.

Loop Diuretics: furosemide, bumetanide, ethacrynic acid

Salicylates (aspirin and quinine), NSAIDs

Antibiotics that end in -mycin or -micin: aminoglycosides (gentamicin), vancomycin, erythromycin

Chemotherapeutic agents: vincristine, vinblastine, cisplatin, carboplatin

Topical agents: ethanol, polymixin B, neomycin

Sudden Hearing Loss Differential Diagnosis 

Occurs over the span of three days.

Differential Diagnosis categories for any ailment can be remembered by the mnemonic VINDICATE

  • Vascular – sickle cell, polycythemia
  • Infectious/Inflammatory – viruses (zoster oticus or herpes, EBV, CMV, mumps), syphilis, labyrinthitis, temporal arteritis
  • Neoplasms – leukemia, masses,  acoustic neuroma
  • Drugs –  loop diuretics, antibiotics that end in -mycin or -micin (aminoglycosides like gentamicin, vancomycin, erythromycin), salicylates and NSAIDs, chemotherapeutic agents (cisplatin, carboplatin, vinblastine, vincristine, and topical agents (ethanol, polymyxin B, neomycin)
  • Iatrogenic/idiopathic – perforated TM, idiopathic endolymphatic hydrops (Meniere’s disease) – vertigo, hearing loss, tinnitus
  • Autoimmune -granulomatosis with polyangitis (Wegener’s)
  • Trauma – ruptured TM
  • Endocrine – diabetes, high cholesterol

Necrotizing Otitis Externa (Malignant Otitis Externa) – an infection that can turn into osteomyelitis of the skull

Presentation: otalgia, headache, and swelling and tenderness around the ear particularly in the setting of a prolonged course of otitis externa.  Diagnosis often requires CT scan to gauge involvement.

Epidemiology: Diabetics, immunocompromised

Etiology: Pseudomonas (90%)
Treatment:   Pediatrics- imipenem or an aminoglycoside and an antispeudomonal penicillin.  Adults – cephalosporin or quinolone

Dispo: Mild cases with good follow up can get oral quinolones as outpatients. More severe cases – admission, IV antibiotics, and perhaps surgical debridement.

Generously donated Rosh Review questions (scroll for answers)

Question 1.[polldaddy poll=8093105]Screen Shot 2014-06-01 at 9.28.25 PM

Question 2.

A 36-year-old woman presents to the ED complaining of decreased hearing and increased fullness to the right ear. Over the last week, she has used cotton-tipped applicators to attempt to remove cerumen from her right ear. On exam, you notice a cerumen-impacted external canal on the right. You irrigate the right ear with warm saline using an 18-gauge IV catheter and a plastic curette to remove the cerumen. During the procedure, the patient has sudden and complete hearing loss to the right ear. [polldaddy poll=8093098]

 

Question 3. A 16-year-old girl presents complaining of pain behind her left ear. She thought the pain was due to an ear infection and took three of her boyfriend’s leftover antibiotic tablets without seeing her primary care physician. Her ear pain improved for a couple of days, but now she is complaining of fever and discharge from the external auditory canal. Her vitals are T 38.4°C, BP 120/80, HR 108, and RR 18. On physical examination, she has postauricular tenderness, swelling, and erythema. You note purulent otorrhea through a perforated tympanic membrane. [polldaddy poll=8096505]

Answers:

1. D-Bullous myringitis was previously linked to Mycoplasma pneumoniae but it appears, based on middle ear aspirate culture results, that typical acute otitis media pathogens are the true cause. Among these, Streptococcus pneumoniae is most common.
2. C – The patient does not require admission (A) to the hospital. ENT care can be arranged for as an outpatient. Traumatic tympanic membrane perforations do not require otic antibiotics (B) unless the ear was contaminated such as from diving in seawater or the rupture is secondary to infection. The patient should receive more than ac otton ball (D) in her ear. Her management should include analgesia and ENT follow-up because complications of tympanic membrane rupture include facial nerve palsy, vertigo, and hearing loss.

3. C – This patient has necrotizing otitis externa.

References:

Silverberg M, Lucchesi M.  Common Disorders of the External, Middle, and Inner Ear.  Tintinalli’s Emergency Medicine, A Comprehensive Study Guide, ed 7. New York, McGraw-Hill, 2011, (Ch) 237:p 1556-1557.