BY KIRSTEN FILL; JAMES MACGREGOR; ANDREW VICTOR; & AHMED RAZIUDDEN, MD
A 32-year-old man was found unresponsive at home by his mother who immediately called the paramedics. The patient was in asystole upon their arrival, and CPR/ACLS protocol was started along with intubation. The patient was transported to the hospital, where ACLS protocol was continued and eventually resulted in the return of a stable pulse. The patient had a significant history of alcohol abuse resulting in liver disease, but had no prior episodes of such events. He also was a smoker of tobacco and marijuana. The patient's mother reported that he had had dark, tarry, melanotic stools and palpitations beginning a few days prior to his unresponsive episode.
The EMT on site administered 6 amps of epinephrine, 2 mg of naloxone, 1 amp of bicarbonate, and D50 via intraosseous line. Resuscitation continued in the ED with another 4 amps of epinephrine administered, resulting in a pulse being re-established. Two peripheral intravenous lines and a subclavian line were then placed to maintain the patient hemodynamically.
The patient was transfused a unit of O negative blood along with a bicarbonate bolus. This allowed for blood to be drawn for tests, and a CBC, CMP, troponin, lactic acid, arterial blood gas, urine analysis, and toxicology screens were ordered. A unique clinical finding in this patient was that the fluid aspirated into the catheter lumen appeared serosanguinous (like pink water) when the central access line was placed, raising the question of whether the catheter was appropriately placed in the subclavian vein.
The blood results correlated with the observed findings in reporting a hemoglobin level of 1.2 g/dL with a hematocrit value of 6.3% and a normal MCV. The patient was found to be acidotic with a pH value of < 6.8, lactic acid of 20.5 mmol/L, troponin elevated at 0.166 ng/mL, and ammonia at 473.3 ug/dL. The patient's WBC count was elevated at 16,260, but the rest of his laboratory workup was relatively normal except for mildly elevated LFTs. The patient's stool sample was melanotic and tested heme-positive.
Despite continued maintenance efforts, the patient eventually expired later in the ICU before further workup could be done to explain the cause of his sepsis and dramatically low hemoglobin value. This raises the question of how low a hemoglobin value can be while sustaining life in a normal individual.
Anemia in Alcoholics
Hemoglobin levels of less than 13.5 g/dL in men and less than 12.0 g/dL in women defines anemia. Anemia in chronic alcoholics is often multifactorial and involves poor nutrition, chronic inflammation, blood loss, liver dysfunction, and ineffective erythropoiesis. (Medicine [Baltimore] 1986;65:322.) Alcohol also has direct toxic effects on the bone marrow red blood cell production as well as red blood cell functionality and lifespan. The table summarizes contributory factors to anemia in alcoholics.
Factors causing anemia in chronic alcoholics.
Physiologic mechanisms will compensate for the decrease in red blood cell mass primarily by alterations in hemoglobin oxygen affinity, blood flow redistribution, and cardiac output adjustments. These mechanisms work in unison to attempt adequate oxygenation, butthe body cannot decrease its tissues' oxygen requirement.
Increases in oxidative metabolism occur as a consequence of the energy required for the compensatory activities. The severity of the clinical presentation relates less to the hemoglobin level and more to the length of time in which the condition develops. Anemias that develop over years will allow the compensatory mechanisms to maintain the patient in an asymptomatic state despite a greater RBC mass loss than an acute hemorrhage. (http://bit.ly/2eOTUCL.)
Normochromic normocytic RBC on peripheral smear.
* Hemoglobin oxygen affinity: Anemic blood undergoes an increased extraction of oxygen from tissues, increasing the deoxyhemoglobin in the RBC. The hemoglobin-oxygen curve is shifted to the right due to an increased production of 2,3-diphosphoglycerate. The overall decrease in hemoglobin oxygen affinity improves oxygen delivery to target tissues.
* Blood flow redistribution: Chronic anemic states cause selective vasoconstriction of vessels supplying the kidneys and non-vital areas of the body such as cutaneous sites leading to the clinical finding of pallor. Chronic anemic patients will also paradoxically increase total blood volume due to a plasma volume expansion despite the decrease in RBC mass.
* Increased cardiac output: Severe anemics (Hgb < 7 g/dL) will compensate for tissue hypoxia by increasing cardiac output. The change in output is counteracted by a lower blood viscosity and decreased peripheral vascular resistance so it does not cause a rise in blood pressure. (Semin Hematol 1980;17:164.)
These mechanisms allow the body to adapt, but at what point are these adaptations no longer adequate to maintain vital organ oxygenation? How low can the hemoglobin fall before life can no longer be sustained? Several case reports have attempted to answer this question. De Araujo Azi, et al., presented a case of a 27-year-old Jehovah's Witness patient who survived a hemoglobin level as low as 1.4mg/dL following surgery for scoliosis without receiving blood transfusions. (Transfusion 2014;54:1153.) Further case reports have suggested that patients have survived with hemoglobin levels below 2.0mg/dL even in the setting of aging comorbidities.
Imaizumi, et al., reported a case of a 61-year-old man with bladder cancer and previous gastrectomy for cancer who survived a preoperative hemoglobin level of 1.8mg/dL. (J Anesth 1999;13:125.) The most dramatic of all cases recorded low hemoglobin values with patient survival occurring intraoperatively during a liver transplant for a patient with hepatocellular carcinoma and decompensated liver failure. This patient was recorded as having a hemoglobin level of 0.6 g/dL with associated ventricular tachycardia, sustained ST depressions, and elevated serum lactate levels. (A A Case Rep 2015;4:132.)
It is clear that the human body has a formidable capacity to heal itself and maintain life in the direst of circumstances. Prolonged episodes of chronic anemia lead to significant changes in body homeostasis, allowing it to operate at critically low values of hemoglobin. Notwithstanding patient comorbidities, the human body may appear relatively asymptomatic while demonstrating dangerously low hemoglobin values. We have seen the body's compensatory mechanisms given these circumstances and confirmed sustainability of life even in unique situations such as severe chronic anemia.