Hypokalemia

Disorders of potassium homeostasis are common electrolyte abnormalities encountered in hospitalized patients. Hypokalemia and hyperkalemia have been estimated to occur in about 21% and 3% of hospitalized patients, respectively; though the morbidity and mortality associated with the latter is significantly higher. Potassium is a predominantly intracellular ion and the understanding of its dynamics between intra- and extracellular fluid milieus, along with its handling by the kidneys, is important in the diagnosis and treatment of potassium disorders. This article aims to provide a clinically relevant update on management of potassium disorders for internists.

Hypokalemia is one of the most frequent electrolyte disorders found in clinical practice. Clinical manifestations include a wide range of signs and symptoms; hence, it can be expressed as a heterogeneous clinical picture, ranging from an asymptomatic manifestation to cardiac arrest [1]. Among these entities, uncommon illnesses do exist, and they must be kept in mind to avoid an incorrect diagnosis. One of these conditions is hypokalemic periodic paralysis (HPP), a rare disorder characterized by episodes of extreme muscle weakness that can progress to paralysis [2].

Potassium (K+) is the predominant intracellular
cation. It is essential to the function of all living cells.
Intracellular K+ concentration is over 30 times its
extracellular concentration. Serum K+ is dependent on
it s intake, excretion, and transcellular distribution.
Most of the body’s K+ is in the muscles. Aldosterone
is the main regulator of K+ renal excretion.
Hypokalemia (serum K+ < 3.5 mEq/l) has multiple
manifestations affecting different organ systems.
Careful history and basic laboratory tests are usually
adequate to diagnose most cases of hypokalemia. K+
should be replaced orally whenever feasible.
Intravenous K+ replacement is needed for emergency
management of hypokalemia and in patients who
cannot take oral potassium.

Pica is the compulsive eating of nonnutritive substances and can have serious medical implications. Although it has been described since antiquity, there has been no single agreed-upon explanation of the cause of such behavior. Databases from MEDLINE and PSYCH-Lit were searched from 1964 to the present to find relevant sources of information using the key words &quot;pica,&quot; &quot;obsessive-compulsive disorder,&quot; &quot;iron-deficiency anemia,&quot; and &quot;nutrition.&quot; Pica is observed most commonly in areas of low socioeconomic status and is more common in women (especially pregnant women) and in children. To our knowledge, the prevalence of pica is not known. Numerous complications of the disorder have been described, including iron-deficiency anemia, lead poisoning, and helminthic infestations. Pica is probably a behavior pattern driven by multiple factors. Some recent evidence supports including pica with the obsessive-compulsive spectrum of disorders. Many differe...

Cushing's syndrome (CS) is a condition caused by prolonged exposure to elevated levels of glucocorticoids either endogenous or exogenous. The most common cause of CS is exogenous and depends on frequency and spectrum of medical condition which require glucocorticoid treatment. Exogenous CS is usually identified on the basis of history and laboratory studies. In our case a 55-year old female presented with complains of generalized weakness, easy fatigability, joint pain, generalized body swelling and facial puffiness with recent history of hypertension and diabetes. On clinical examination, she had truncal obesity moon facies, acanthosis nigricans, truncal obesity, pedal edema and high blood pressure. On enquiry patient gives history consumption of some medications for joint pain since last 6 months. She had persistent hypokalemia and high blood sugars. So, on clinical and biochemical features exogenous CS was suspected. Her morning 8 am serum Cortisol levels were 0.96ug/dl which was strongly suggestive exogenous CS. The patient showed clinical and biochemical improvement after stopping of all other medications.

The development of many electrolyte disturbances in the ICU can be prevented by attention to the use of intravenous fluids and nutrition. Hyponatremia is a relative contraindication to the use of hypotonic intravenous fluids and hypernatremia calls for the administration of water. Formulae have been devised to guide the therapy of severe hyponatremia and hypernatremia. All formulae regard the patient as a closed system, and none takes into account ongoing fluid losses that are highly variable between patients. Thus, therapy of severe hyponatremia and hypernatremia must be closely monitored with serial electrolyte measurements. The significance of hypocalcemia in the critically ill is controversial. Hypokalemia, hypophosphatemia, and hypomagnesemia should be corrected.

Fludrocortisone is recommended in patients with orthostatic hypotension and a benefit has been suggested in hemodialysis patients with severe hypokaliemia. We report 2 patients who suffered from chronic severe perdialytic hypotension resistant to midodrine and who were treated in a long-term period with fludrocortisone. A rise of post-dialytic BP was observed with a decrease of the interdialytic weight gain (IWG). We suggest that the IWG decrease is induced by a lessening of the renin angiotensin aldosterone system that could be less stimulated at the end of the dialysis session because of a better-preserved arterial pressure. The decrease of angiotensin could lessen the feeling of thirst.

Generalised paresis, severe hypokalaemia and kaliuresis, metabolic alkalosis and hypertension, characteristic of mineralocorticoid excess, were identified in a dog with hyperadrenocorticism due to a functional adrenocortical carcinoma. Aldosterone concentration was decreased and deoxycorticosterone concentration increased in the presence of hypokalaemia. These metabolic abnormalities resolved with resection of the carcinoma. Mineralocorticoid excess in dogs with hyperadrenocorticism is generally considered to be of little clinical significance but resulted in the acute presentation of this patient. The possible pathogenesis of mineralocorticoid excess in this case of canine hyperadrenocorticism is discussed.

Abnormal potassium metabolism may contribute to the increased cardiac morbidity and mortality seen in dialysis patients. We studied the pattern of serum potassium levels in a cohort of Chinese peritoneal dialysis (PD) patients. We studied serum potassium levels of 266 PD patients during 3 consecutive clinic visits. Dialysis adequacy, residual renal function, and nutritional status also were assessed. Patients were followed up for 33.7 +/- 20.7 months. Mean serum potassium level was 3.9 +/- 0.5 mEq/L (mmol/L). Five patients (1.9%) had an average serum potassium level less than 3 mEq/L (mmol/L), whereas 54 patients (20.3%) had a serum potassium level less than 3.5 mEq/L (mmol/L). Serum potassium levels correlated with overall Subjective Global Assessment score (r = 0.276; P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.001) and serum albumin level (r = 0.173; P = 0.005) and inversely with Charlson comorbidity score (r = -0.155; P = 0.011). There was no correlation between serum potassium level and daily PD exchange volume, total Kt/V, urine volume, or residual glomerular filtration rate. By means of multivariate analysis with Cox proportional hazard model to adjust for confounders, serum potassium level was an independent predictor of actuarial patient survival. PD patients with hypokalemia (serum potassium &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 3.5 mEq/L [mmol/L]) had significantly worse actuarial survival (hazard ratio, 1.79; 95% confidence interval, 1.12 to 2.85; P = 0.015) than those without hypokalemia after adjusting for confounding factors. Hypokalemia is common in Chinese PD patients. Serum potassium level was associated with nutritional status and severity of coexisting comorbid condition. Furthermore, hypokalemia was an independent predictor of survival in PD patients. Additional studies may be needed to investigate the benefit of potassium supplementation for PD patients with hypokalemia.

The case of an Albanian patient is reported, with bilateral adrenal hyperplasia diagnosed after a condition of persistent hypokalemia, in spite of continuous and adequate potassium administration. The patient, a Caucasian male of middle age, was suffering from diabetes, hypertension and angina pectoris, and admitted in a University Hospital Facility due to an unexplained confusional state. U waves were registered in the electrocardiography, and abdominal imaging was suggestive of adrenal hyperplasia. His plasmatic levels of potassium started to improve and became normal only after a therapy with potassium sparing diuretic, in our case with spironolactone. The administration of this type of drug has been widely advocated even for diagnostic purposes, when an unexplained condition of hypokalemia persists. Our case suggests that in lack of obvious causes of hypokalemia, suspicions on the existence of a primary hyperaldosteronism should be formulated, and investigations or therapeutic i...

C. Barrett Bowling, MD, 1,2 Bertram Pitt, MD, 3 Mustafa I. Ahmed, MD, 1 Inmaculada B. Aban, ... PhD, 1 Paul W. Sanders, MD, 1,2 Marjan Mujib, MBBS, MPH, 1 Ruth C. Campbell, MD, 1 Thomas ... E. Love, PhD, 4 Wilbert S. Aronow,MD, 5 Richard M. Allman, MD, 1,2 ...

Since the initial description in the 1960s of patients with seemingly inherited disorders characterized by hypokalemia and metabolic alkalosis, the pathophysiologic processes underlying Bartter and Gitelman syndromes have generated tremendous study and speculation. Recently described mutations in genes encoding transport proteins important in sodium and chloride reabsorption in the thick ascending limb of Henle and distal convoluted tubule have confirmed these processes as the proximate defects in Bartter and Gitelman syndromes, respectively. Basic understanding of the role of these proteins in normal sodium and chloride homeostasis, and review of the secondary mediators stimulated by loss of their function provide insight into the clinical manifestations and response to treatment observed in these disorders.