EMS World Magazine is the most authoritative source in the world for clinical and educational material designed to improve the delivery of prehospital emergency medical care.
Issue link: https://emsworld.epubxp.com/i/697542
EMSWORLD.com | JULY 2016 15 C e n t r a l P o n t i n e M y e l i n o l y s i s Central pontine myelinolysis, when severe, is known as locked-in syndrome. In locked-in syndrome, the patient loses function to all motor neurons except those that control vertical eye movements, blinking, breathing and alertness. In other words, the patient can see and is completely aware of everything going on but cannot speak or move. The exact mechanism that causes a loss of myelin is unknown, but what is known is that rapidly corrected chronic hyponatremia results in edema of the pons, midbrain, thalamus, basal ganglia and cerebellum. This edema is believed to irreversibly (in the majority of cases) disrupt neuronal function. As a general rule, if sodium concentration is altered over a short period of time, then the sodium/fluid balance should be corrected rapidly. If the sodium concentration is altered over a prolonged period of time (greater than 48 hours), the sodium/fluid balance must be corrected slowly. The exception to this rule is the patient with severe neurologic symptoms such as seizures or severe neurologic dysfunction. Help identify errors and near-miss events that affect the safety of EMS providers and patients by reporting anonymously at www.emseventreport.com. Data collected will be used to develop policies, procedures and training programs. C R M T i p s : D i g D e e p It is easy to get tunnel vision. As in this case, not everything is black and white. We often talk to patients and use information presented on the surface to form our differential diag- noses. In EMS we are constantly mak- ing diagnoses and need to be well informed to make the best decision possible for our patients. so excessively that his friends started call- ing him "the whiz kid." Pathophysiology In hot conditions where dehydration is like- ly, it is important to remember that people will normally slow or stop their urinary out- put. This forces reabsorption of water. This mechanism is designed to prevent further dehydration and ensure the kidneys do not eliminate the much-needed fluid. This mechanism is regulated by the renin- angiotensin-aldosterone system. It works by identifying the sodium (salt) level in the blood and either activating the system when the salt level is too high or turning it off if the salt level is too low. This is a complex process but can be simplified (not the most physio- logically accurate statement but an example that it is easy to understand) by saying that high salt makes the blood thick, and low salt will conversely make it thin. The body never likes extremes and will do everything pos- sible to exist in a perfectly balanced state. The hormone that is primarily respon- sible for regulating water in the kidneys is antidiuretic hormone, more commonly known as ADH. When ADH is present it will stop diuresis (urinary excretion). Alcohol Efects This is where things get really interesting. Have you ever heard someone say, "Don't break the seal" when they have been drink- ing alcohol? This is a metaphorical "seal"; there is no physiologic basis for it. This incessant need to continue to pee after the seal is broken is a direct result of the loss of control by ADH. Alcohol directly blocks ADH release, and as a result ADH no longer regulates urinar y excretion. Despite the fact that alcohol, by its nature, dehydrates the blood, there is no hormon- al protection from dehydration. Increases in urinary output caused by ADH block- ade and chemical dehydration caused by alcohol will lead to less water available to dilute the high salt content of the blood. After further evaluating the patient in the medical tent, the physician reported an initial i-STAT POCT blood sodium (salt) level of 118 milliequivalents per liter (mEq/L). The normal blood sodium level is between 135–145 mEq/L. This finding in itself would be concerning and under normal circumstances associated with an increase in blood volume. An increase in blood volume will cause dilution of the sodium and ultimately lead to a relative hyponatremia. However, this patient was exhibiting clinical signs of decreased blood volume. There are a few steadfast rules of phys- iology, and one of them is that sodium always follows water. Wherever water goes, it drags sodium with it. In this case the patient was dangerously hyponatremic. Continuing to give him more fluids without managing his sodium was extremely risky. The patient was transported to the ED, and his clinical picture remained unchanged despite conservative fluid resuscitation strategies. Fluid resuscitation was approached conservatively to ensure that permanent neurologic damage was not caused by the paramedics (see central pontine myelinolysis sidebar). The key lesson in this case with is to keep a high index of suspicion and listen to the patient. Many times prehospital care pro- viders will be the only medically trained providers to see the scene and talk to bystanders. Being a good differential diag- nosis "detective" will save many patients. Editor's note: Cases are obfuscated and amalgamated to protect patient privacy and provider anonymity. While staying as true as possible to the actual event, creative license is used to better explain the lesson(s) in the case. ABOUT THE AUTHORS David Page, MS, NRP, is director of the Prehospital Care Research Forum at UCLA. He is a senior lecturer and PhD candidate at Monash University. He has over 30 years of experience in EMS and continues to be active as a field paramedic for Allina Health EMS in the Minneapolis/St. Paul area. Will Krost, MD, MBA, NRP, is a faculty member at the George Washington University School of Medicine and Health Sciences in the Departments of Clinical Research and Leadership and Health Sciences. He has over 23 years of experience in EMS operations, critical care transport and hospital administration.