The Bottom Line: Staphylococcus aureus is the main cause of septic arthritis involving native joints, although many other organisms are encountered also. In our center, neither the distribution nor the antibiotic susceptibility profiles of the causative organisms changed significantly over the last 30 years.
Table 1 Organisms responsible for septic arthritis. Page 439
Dubost, J., Couderc, M., Tatar, Z., Tournadre, A., Lopez, J., Mathieu, S., & Soubrier, M. (2014). Three-decade trends in the distribution of organisms causing septic arthritis in native joints: Single-center study of 374 cases. Joint, Bone, Spine, 81(5), 438-440.
In this study, the distribution and antibiotic susceptibility profile of the organisms responsible for septic arthritis showed little change over the 30-year study period. Importantly, no significant increase in MRSA was noted, in keeping with a previous study. These findings do not support the use in our center of broader-spectrum antibiotics in patients for whom empirical antibiotic therapy is deemed necessary.
How to remove a tick
Centers for Disease Control and Prevention June 1, 2015
Use fine-tipped tweezers to grasp the tick as close to the skin’s surface as possible.
Pull upward with steady, even pressure. Don’t twist or jerk the tick; this can cause the mouth-parts to break off and remain in the skin. If this happens, remove the mouth-parts with tweezers. If you are unable to remove the mouth easily with clean tweezers, leave it alone and let the skin heal.
After removing the tick, thoroughly clean the bite area and your hands with rubbing alcohol, an iodine scrub, or soap and water.
Dispose of a live tick by submersing it in alcohol, placing it in a sealed bag/container, wrapping it tightly in tape, or flushing it down the toilet. Never crush a tick with your fingers.
The Bottom Line: Jaundice occurs when there are disruptions along this metabolic pathway, causing an increase in unconjugated bilirubin (e.g., from increased red blood cell destruction or impaired bilirubin conjugation) or conjugated bilirubin.
Figure 1. An algorithmic approach to the evaluation of jaundice in adults page 165
Fargo, M., Grogan, S., & Saguil, A. (n.d.). Evaluation of Jaundice in Adults. American Family Physician., 95(3), 164-168.
Unconjugated hyperbilirubinemia occurs with increased bilirubin production caused by red blood cell destruction, such as hemolytic disorders, and disorders of impaired bilirubin conjugation, such as Gilbert syndrome. Conjugated hyperbilirubinemia occurs in disorders of hepatocellular damage, such as viral and alcoholic hepatitis, and cholestatic disorders, such as choledocholithiasis and neoplastic obstruction of the biliary tree.
The Bottom Line: Against a fundamental contribution for IL-6 in Stauffer’s syndrome is the wide variety of circumstances in which its elevation has no association with inflammatory or cholestatic liver disease. Nevertheless, dysregulated Il-6 acting through disparate signaling cascades is implicated in a variety of autoimmune and inflammatory conditions
Gremida, A., Al-Taee, A., Alcorn, J., & McCarthy, D. (n.d.). Hepatic Dysfunction in Renal Cell Carcinoma: Not What You Think? Digestive Diseases and Sciences., Digestive diseases and sciences. , 2017.
Although the pathophysiology of Stauffer’s syndrome has not been clearly elucidated, tumor overexpression of interleukin 6 (IL-6) is present in 50–80% of patients with RCC and has been suggested as a possible causative factor in one report
Bottom Line: An analysis of FDA Adverse Event Reporting System (FAERS) data and three case reports provide evidence that sodium glucose cotransporter 2 (SGLT2) inhibitors (canagliflozin, dapagliflozin, and empagliflozin) cause ketoacidosis.
A search was done of the FAERS data for “reports of acidosis in patients treated with canagliflozin, depagliflozin, or empagliflozin,” and the number of those reports was compared to acidotic reports for those treated with sitagliptin and saxagliptin, the two most commonly used DPP4 (dipeptidyl peptidase 4) inhibitors. The investigators made estimates of patient exposure and concluded that the “overall risk of developing acidosis was ~14-fold higher for SGLT2 inhibitors….After excluding patients with T1D [type 1 diabetes] and focusing on patients identified as having T2D [type 2 diabetes], we estimate that SGLT2 inhibitors were associated with ~7-fold increase in developing acidosis. Seventy-one percent had euglycemic ketoacidosis.”
Reference: Blau, J. E., Tella, S. H., Taylor, S. I., & Rother, K. I. (2017). Ketoacidosis and SGLT2 inhibitor treatment: Analysis of FAERS data. Diabetes/Metabolism Research and Reviews. [Epub ahead of print]. doi: 10.1002/dmrr.2924. PMID: 28736981.
Three case reports
- Wang, A. Y., Hou, S. K., & Li, S. J. (2017). Euglycemic diabetic ketoacidosis in type 2 diabetes with sodium glucose cotransporter 2 inhibitors. The American Journal of Emergency Medicine, 35(2), 379.e5-379.e6. doi: 10.1016/j.ajem.2016.08.055. PMID: 27614369. Discusses the case of a 61-year-old woman with a history of type 2 diabetes for 10 years who went to the emergency department because of severe vomiting for a day. She started taking empagliflozin a few days prior to ED visit due to “unsatisfactory sugar control.” Treatment consisted of IV fluid, an IV insulin pump, and a dextrose infusion for hypoglycemia prevention.
- Ghosh, A., Gupta, R., & Misra, A. (2016). Ketonuria/ketonemia associated with the use of sodium-glucose cotransporter 2 (SGLT-2) inhibitors in type 2 diabetes: A report of three cases from New Delhi, India. Journal of Diabetes, 8(5), 738-739. doi: 10.1111/1753-0407.12411. PMID: 27085074. Abstract is not in PubMed. To view the article, click on the link to it and then click “Request via ILLiad” to request the full text via interlibrary loan; one must create an ILLiad account the first time the service is used. You will receive an email notification when full-text article has been uploaded into your account.
- Rashid, O., Farooq, S., Kiran, Z., & Islam, N. (2016). Euglycaemic diabetic ketoacidosis in a patient with type 2 diabetes started on empagliflozin. BMJ Case Reports. doi: 10.1136/bcr-2016-215340. PMID: 27177938. Discusses the case of a 42-year-old man with type 2 diabetes who went to the emergency room because of nausea, vomiting, and abdominal pain. “He had recently changed his diabetes medications and started on an SGLT2 inhibitor (empagliflozin) along with metformin, pioglitazone, liraglutide and self-adjusted exogenous insulin.” Article discusses link between SGLT2 inhibitors and DKA and also covers euglycaemic diabetic ketoacidosis’ pathophysiology. To view the article, click on the link to it and then click “Request via ILLiad” to request the full text via interlibrary loan; one must create an ILLiad account the first time the service is used. You will receive an email notification when full-text article has been uploaded into your account.
Bottom Line: Causes of anion gap metabolic acidosis are broken down into the following categories: overproduction of acid due to ketoacidosis or lactic acidosis, underexcretion of acid (such as due to advanced renal failure/chronic kidney disease (uremia)), cell lysis (such as due to massive rhabdomyolysis, penicillin-derived antibiotics, and pyroglutamic acid (5-oxoproline). Two mnemonics for remembering the causes are GOLDMARK and CAT MUD PILES.
Here is the full listing of causes from DynaMed Plus → Anion gap metabolic acidosis → Etiology and pathogenesis → Causes.
- overproduction of acid, such as due to
- uncontrolled diabetes
- alcoholic ketoacidosis
- starvation ketoacidosis
- life-threatening ketoacidosis reported following strict adherence to Atkins diet (maintaining ketonuria for 1 month) in case report
- inactivating mutations in monocarboxylate transporter 1 associated with increased ketoacidosis severity in genetic analysis of 96 patients
- lactic acidosis
- type A L-lactic acidosis – hypoxic lactic acidosis, causes include
- septic shock
- hypovolemic shock
- acute mesenteric ischemia
- cyanide poisoning
- carbon monoxide poisoning
- type B L-lactic acidosis – nonhypoxic lactic acidosis, causes include
- thiamine deficiency
- poor lactate clearance due to liver failure
- glycogen storage diseases
- malignancy such as Hodgkin lymphoma (HL)
- medications and drugs
- nucleoside reverse transcriptase inhibitors
- isoniazid toxicity
- iron toxicity
- aspirin intoxication
- ethanol intoxication (different than alcoholic ketoacidosis)
- methanol poisoning
- isopropyl alcohol poisoning
- ethylene glycol poisoning
- paraldehyde poisoning
- propylene glycol intake
- early toluene intake
- underexcretion of acid, such as due to advanced renal failure/chronic kidney disease (uremia)
- cell lysis, such as due to massive rhabdomyolysis
- penicillin-derived antibiotics
- pyroglutamic acid (5-oxoproline)
Reference: DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 116876, Anion gap metabolic acidosis; [updated 2015 Oct 27, cited 2017 Aug 3].
Provided by Dr. David Krakow
- G – glycols -ethylene glycol ( antifreeze) and propylene glycol (solvent for lorazepam among other uses)
- O – oxoproline (tylenol use in sick, malnourished patient)
- L – L Lactate
- D – D Lactate (consider in patient with risk for bacterial overgrowth who gets confused after carbohydrate load)
- M – methanol
- A – aspirin (salicylates)
- R – renal failure
- K – ketoacidosis (DKA, AKA, starvation ketoacidosis)
From DynaMed Plus → Anion gap metabolic acidosis → Etiology and pathogenesis → Causes.
CAT MUD PILES
- C – carbon monoxide, cyanide
- A – alcoholic ketoacidosis (starvation ketoacidosis)
- T – toluene (can cause both normal anion gap and elevated anion gap acidosis)
- M – methanol, metformin
- U – uremia
- D – diabetic ketoacidosis
- P – propylene glycol, paraldehyde, phenformin
- I – isoniazid, iron
- L – lactic acidosis
- E – ethylene glycol, ethanol
- S – salicylates