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Hypokalemic paralysis is a clinical syndrome characterized by acute flaccid paralysis with concomitant hypokalemia. Complications, such as acute respiratory failure and cardiac arrhythmias, can be fatal. If treated appropriately, the patient can recover without any sequelae. We present a rare case of life-threatening hypokalemic paralysis following the ingestion of an unknown substance. At presentation, her serum potassium concentration was 1.9 mmol/L. A review of the patient's history confirmed the ingestion of barium chloride. She was diagnosed with acute barium poisoning characterized by high serum and urine barium levels. Aggressive potassium repletion was administered intravenously and orally. Her serum potassium concentration dropped to 1.5 mmol/L and peaked at 5.4 mmol/L following treatment. The patient achieved a complete recovery and was discharged without sequelae. Barium can competitively block the potassium inward rectifier channels and interfere with the efflux of intracellular potassium, leading to severe hypokalemia. Our report illustrates a rare presentation of acute barium intoxication and a differential diagnosis indicating hypokalemic paralysis. We also discuss the pathophysiological features and compare the clinical findings with cases of rebound hyperkalemia. [ABSTRACT FROM AUTHOR]

Dengue infection is a mosquito borne arboviral disease of the tropics. It has a wide spectrum of presentation from flu-like illness to lethal hemorrhagic fever. Neurological manifestations are rare in dengue and can be due to neurotropic effect, immune mediated, or due to systemic complication. We hereby present a case report of a 21-year-old male presenting to us with acute pure motor quadriparesis due to hypokalemia caused by dengue fever.

Glucocorticoid resistance syndrome is a rare disorder with no genetically proven cases reported from India; in addition, there are no descriptions available regarding its management during pregnancy. A 27-year-old woman, hypertensive since the age of 17 years, presented with hypokalemic paresis. She reported regular menses and acne. On investigation, she had elevated serum cortisol that remained unsuppressed after a low-dose dexamethasone suppression test. Genetic analysis revealed a novel, homozygous missense variant in exon 5 of the NR3C1 gene confirming glucocorticoid resistance syndrome. She was managed with oral dexamethasone followed by tapering of antihypertensive drugs. A year later, she conceived with assisted reproductive techniques when dexamethasone was replaced with prednisolone, necessitating the reintroduction of antihypertensive drugs to maintain normotension and potassium supplements to manage hypokalemia. She presented with acute abdomen at 36 weeks of gestation; evaluation revealed right adrenal hemorrhage, which was managed conservatively. Postpartum, the right adrenal lesion reduced in size and an underlying right adrenal myelolipoma was unveiled. [ABSTRACT FROM AUTHOR]

Dengue infection is a mosquito borne arboviral disease of the tropics. It has a wide spectrum of presentation from flu-like illness to lethal hemorrhagic fever. Neurological manifestations are rare in dengue and can be due to neurotropic effect, immune mediated, or due to systemic complication. We hereby present a case report of a 21-year-old male presenting to us with acute pure motor quadriparesis due to hypokalemia caused by dengue fever. [ABSTRACT FROM AUTHOR]

Hypokalemic paralysis is a clinical syndrome characterized by acute flaccid paralysis with concomitant hypokalemia. Complications, such as acute respiratory failure and cardiac arrhythmias, can be fatal. If treated appropriately, the patient can recover without any sequelae. We present a rare case of life-threatening hypokalemic paralysis following the ingestion of an unknown substance. At presentation, her serum potassium concentration was 1.9 mmol/L. A review of the patient’s history confirmed the ingestion of barium chloride. She was diagnosed with acute barium poisoning characterized by high serum and urine barium levels. Aggressive potassium repletion was administered intravenously and orally. Her serum potassium concentration dropped to 1.5 mmol/L and peaked at 5.4 mmol/L following treatment. The patient achieved a complete recovery and was discharged without sequelae. Barium can competitively block the potassium inward rectifier channels and interfere with the efflux of intracellular potassium, leading to severe hypokalemia. Our report illustrates a rare presentation of acute barium intoxication and a differential diagnosis indicating hypokalemic paralysis. We also discuss the pathophysiological features and compare the clinical findings with cases of rebound hyperkalemia.

Aim: To describe the clinical and laboratory features of Sjögren's syndrome (SS) with renal tubular acidosis (RTA) from published literature. Methods: A systematic search of indexed publications in all languages till December 2021 identified cases of SS with RTA (SS‐RTA) and were included if either antibody (anti‐SSA/anti‐SSB) or salivary gland histopathology were positive. Results: There were 440 cases of SS‐RTA (63.9% from Asia, 95.5% women). The median (range) age was 37 (6‐78) years. Only 7.7% had a previous diagnosis of SS. Oral or ocular sicca symptoms were present in 63.7%. Positive ocular tests, oral tests, anti‐SSA, anti‐SSB and salivary gland histopathology were reported in 256/331 (77.3%), 123/128 (96%), 382/407 (93.9%), 298/379 (78.6%), and 246/268 (91.8%), respectively. Hypokalemic paralysis (HP) was the presenting feature in 63.6%; 25% had multiple episodes of HP and 8.4% had respiratory paralysis. Type 1, type 2, combined type 1 & 2, and type 4 RTA was seen in 388, 8, 38, and 3 patients, respectively. Proximal dysfunction and RTA complications were infrequently evaluated. Fanconi syndrome, nephrogenic diabetes insipidus, proteinuria, and low estimated glomerular filtration rate were found in 45, 21, 178, and 157, respectively. Nephrocalcinosis, renal stones, and osteomalacia were reported in 92, 79, and 72, respectively. Tubulointerstitial nephritis was found in 142 out of 152 renal biopsies. Conclusion: SS‐RTA is an early manifestation of SS characterized by younger age and subclinical sicca symptoms. Although evaluated less frequently, oral sicca signs and salivary gland biopsy have a high positive yield. HP is the most common presentation. RTA is mostly distal; proximal dysfunction and complications were infrequently assessed. [ABSTRACT FROM AUTHOR]

Background Disorders of consciousness (DOC) are neurocognitive disorders related to sharp fluctuations of attention and consciousness, while DOC is characterized by significant interindividual differences, rapid development, and a higher lethal rate. Case information A 53‐year‐old female patient underwent general anesthesia with tracheal intubation in otoendoscopic tympanoplasty. The patient suddenly appeared moderate DOC after tracheal tube removal with K+ 3.6 (3.5–5.3 mmol/L). Based on the ancillary testing and routine laboratory workup, the possible causes of DOC, such as general anesthesia drugs and cardio cerebral events, were temporarily excluded. DOC was reversed by intravenous administration of KCl 1 g, with K+ 3.78 mmol/L. On one day after surgery, the patient occurred suddenly DOC again after intravenous guttae of 5% glucose 1000 ml, K+ 3.87 mmol/L, possibly because of her recurrent hypokalemic paralysis (HP) of past medical history. The patient's consciousness gradually improved after effective KCl supplementation therapy. Conclusion DOC caused by periodic paralysis (PP) has not been reported, we speculate that hypoactive DOC is closely correlated with normokalemic periodic paralysis (NormoPP) in this case.

Introduction: Neurological manifestation of dengue virus infection is a rare entity. Serotypes commonly associated with neurological manifestation are DENV-2 and DENV-3. We plan to detect the serotypes related to the neurological presentation in dengue infection and its correlation with different neurological complications and outcome. Methods: In this case–control study, consecutive dengue cases with different neurological manifestations were enrolled along with age and sex-matched controls (dengue patients without neurological complication). Serotyping using RT-PCR of samples of cases and controls were done. Level of correlation was analyzed with various parameters and outcomes. Results: In cases out of 33 samples, 6 sample serotypes were detected, which were composed of DENV-1 (n = 2) and DENV-2 (n = 4). In controls, DENV-1 (n = 5), DENV-2 (n = 6), and DENV-3 (n = 3) were detected. When statistically correlated, no significant association was found in cases and controls with dengue virus serotype. The frequency of serotype 2 was higher in hypokalemic paralysis cases than non-hypokalemic paralysis cases and the difference was significant (p < 0.05). The outcome was good (mRS < 3) in all the cases where serotypes were detected, but on statistical correlation, it was not found significant (p > 0.05). Conclusion: DENV-1 and DENV-2 are associated with neurological manifestation of dengue infection, which is different from the existing literature, where DENV-2 and DENV-3 are reported. The detection of DENV serotype will help in predicting and best management of neurological complication. The serotype 2 of dengue virus is more commonly associated with dengue-associated hypokalemic paralysis than other neurological complication (p < 0.05). There is no significant association of serotypes with outcome or mortality. [ABSTRACT FROM AUTHOR]

Abstract Background Familial distal renal tubular acidosis (dRTA) associated with mutations of solute carrier family 4 membrane − 1 (SLC4A1) gene could co-exist with red cell membrane abnormality, Southeast Asian ovalocytosis (SAO). Although this association is well described in Southeast Asian countries, it is less frequently found in Sri Lanka. Case presentation We describe six patients who had dRTA co-existing with SAO. All of them initially presented with severe hypokalemia and paralysis. They presented within a period of six months to the Teaching Hospital Anuradhapura, Sri Lanka. All had metabolic acidosis indicated by low serum bicarbonate. Three of them were having underlying chronic kidney disease as well. Those three patients had mixed high and normal anion gap metabolic acidosis indicated by low delta ratio. In all dRTA was confirmed by presence of normal anion gap, hyperchloraemia, high urine pH and positive urine anion gap. Examination of blood films of all of them revealed presence of stomatocytes and macro-ovalocytosis compatible with SAO. In relation to complications of dRTA, two patients had medullary nephrocalcinosis. Three patients had biochemical evidence of osteomalacia, with two of them having radiological evidence of diffuse osteosclerosis. One patient had secondary hyperparathyroidism and a pathological fracture. Conclusions Erythrocyte in SAO is exceptionally rigid and this abnormality is said to be evolved as it protects against Plasmodium vivax malaria and cerebral malaria cause by Plasmodium falciparum. Although two families of SAO was described earlier, SAO and dRTA combination was reported only once in a patient from Anuradhapura district. Distal renal tubular acidosis, SAO combination and its related complications including nephrocalcinosis, chronic kidney disease and metabolic bone disease was not described in Sri-Lankan literature. This case series emphasize the importance of investigating recurrent/ chronic hypokalemia to diagnose dRTA and its associations, as early correction of acidosis could prevent development of chronic kidney disease and metabolic bone disease.

The article provides answers to the possible diagnosis and treatments of a 12-year-old female with hypokalemic paralysis and discolored teeth, including her diagnosis of normal anion gap metabolic acidosis (NAGMA) with hypokalemia and possible treatments like oral potassium supplements.

With an ever-increasing trend in the side effects of antiretroviral therapy (ART), usage of new regimens to decrease the mortality and morbidity has come into picture. Here we report a case of tenofovir-induced hypokalemic paralysis. A 60-year-old female patient came to a medical outpatient department with quadriparesis. History revealed that she was diagnosed with HIV 6 years back and was on zidovudine, lamivudine, and efavirenz. Three months later, she developed severe anemia because of which zidovudine was replaced by tenofovir. On evaluation, there was hypokalemia with appropriate electrocardiography changes. As previous literature showed association of hypokalemia with tenofovir, we attributed this finding to the usage of tenofovir. ART was stopped, and the patient was given potassium supplements and potassium-rich diet. There was dramatic improvement with the treatment and the patient regained muscle strength. After 1 week, she was put on other alternative regimen consisting of abacavir, lamivudine, and efavirenz. Her CD4 count was improved without any complaints. The patient was monitored on outpatient basis in ART center.

Background: Familial distal renal tubular acidosis (dRTA) associated with mutations of solute carrier family 4 membrane - 1 (SLC4A1) gene could co-exist with red cell membrane abnormality, Southeast Asian ovalocytosis (SAO). Although this association is well described in Southeast Asian countries, it is less frequently found in Sri Lanka.Case Presentation: We describe six patients who had dRTA co-existing with SAO. All of them initially presented with severe hypokalemia and paralysis. They presented within a period of six months to the Teaching Hospital Anuradhapura, Sri Lanka. All had metabolic acidosis indicated by low serum bicarbonate. Three of them were having underlying chronic kidney disease as well. Those three patients had mixed high and normal anion gap metabolic acidosis indicated by low delta ratio. In all dRTA was confirmed by presence of normal anion gap, hyperchloraemia, high urine pH and positive urine anion gap. Examination of blood films of all of them revealed presence of stomatocytes and macro-ovalocytosis compatible with SAO. In relation to complications of dRTA, two patients had medullary nephrocalcinosis. Three patients had biochemical evidence of osteomalacia, with two of them having radiological evidence of diffuse osteosclerosis. One patient had secondary hyperparathyroidism and a pathological fracture.Conclusions: Erythrocyte in SAO is exceptionally rigid and this abnormality is said to be evolved as it protects against Plasmodium vivax malaria and cerebral malaria cause by Plasmodium falciparum. Although two families of SAO was described earlier, SAO and dRTA combination was reported only once in a patient from Anuradhapura district. Distal renal tubular acidosis, SAO combination and its related complications including nephrocalcinosis, chronic kidney disease and metabolic bone disease was not described in Sri-Lankan literature. This case series emphasize the importance of investigating recurrent/ chronic hypokalemia to diagnose dRTA and its associations, as early correction of acidosis could prevent development of chronic kidney disease and metabolic bone disease. [ABSTRACT FROM AUTHOR]

Introduction: Hypokalemia is associated with increased morbidity and at times mortality. “Hypokalemic paralysis”, particularly if recurrent, has often been considered synonymous with “hypokalemic periodic paralysis (HPP)”; however, diseases such as Gitelman syndrome (GS), Bartter syndrome (BS), and renal tubular acidosis (RTA) can have identical presentation. We have tried to explore the etiological spectrum along with epidemiological and certain clinical, biochemical, and electrophysiological features in patients with hypokalemic paralysis. Materials and Methods: In this observational study, 200 appropriate patients with hypokalemic paralysis (serum K+ 25 mmol/day as the cutoff for inappropriate renal loss of potassium in presence of hypokalemia. Serum and urinary osmolality along with arterial blood gas analysis were performed in all patients with renal loss of potassium. Serum and urinary sodium, potassium, calcium, magnesium, chloride, and creatinine were measured in normotensive patients with metabolic alkalosis. Hypertensive patients were evaluated with plasma aldosterone and renin activity. Results: Probable GS topped the list involving 28% individuals of the entire cohort while probable BS, distal RTA, and HPP were diagnosed in 20%, 22%, and 19% cases, respectively. Rural tribal population (61%) and age group of 30–40 years suffered the most (48%) with concentration of cases in hot and humid summer months. Conclusions: We suggest that patients with hypokalemic paresis should be evaluated thoroughly to unmask the underlying etiology that may have a different therapeutic and prognostic connotations and not to use the term “periodic” in cases of recurrent hypokalemic paralysis.

Hypokalemic periodic paralysis is anautosomal dominantdisease characterized by muscle weakness or paralysis with a matching fall in blood potassium levels. Paralysis attacks often occur in adolescence and are induced by strenuous exercise followed by rest, high carbohydrateor high sodiummeal content, sudden changes in temperature, and even excitement, noise, flashing lights and cold temperatures. Despite global daily use of intravenous and oral potassium in the treatment of patients, data about intravenous bolus potassium is rare. Here we report a 29-year-old man complaining of weakness in the upper and lower limbs. By initial diagnosis of periodic hypokalemic paralysis, potassium chloride was ordered by oral route. After a few minutes, we heard patient screaming in pain. He complained of severe acute pain in peripheral intravenous line, palpitation and dyspnea. We noticed that potassium chloride vial was infused directly via cubital vein in few minutes erroneously. Physical exam revealed sinus tachycardia and hypertension. We began hyperkalemia treatment immediately. With appropriate treatment,the patient was discharged with good condition after 12 hours of admission.

Endocrine disorders affect mobility in many and sometimes characteristic ways such as Cushing's syndrome or hyperparathyroidism, which have direct, hormone-mediated effects on skeletal and muscular tissues. On the other hand, the endocrine system plays an important role in the development of (osteo)sarcopenia, the meaning of which is increasingly recognized in the prognosis of various diseases. Conversely, lack of physical activity is crucial in the development of metabolic diseases, which are associated with serious individual and socio-economic consequences. [ABSTRACT FROM AUTHOR]

Background and Aims: As a part of Global Polio Eradication Programme by the World Health Organization, 1988 surveillance of acute flaccid paralysis (AFP) was an important public health activity in many countries. With nearing the eradication of poliomyelitis, other causes of AFP are gaining importance in both children and adults. This study was designed to know the clinical characteristics, and differential diagnosis of causes of AFP, including distribution by age, gender, and time. This was a prospective observational study. Methods: AFP cases were diagnosed on the basis of history and physical examination. The underlying etiology was ascertained by appropriate laboratory investigations such as arterial blood gas analysis, urinary pH, electrolytes, thyroid profile, electrophysiological studies, cerebrospinal fluid analysis, and imaging. Results: Between July 2010 and September 2012, 106 cases of AFP were enrolled. Out of 106 patients, 58 (54.7%) were suffering from Guillain-Barrι syndrome (GBS), 15 (14.2%) from hypokalemic paralysis, 8 (7.5%) from myasthenia gravis, 8 (7.5%) from thiamine deficiency, 5 (4.7%) from transverse myelitis, and 2 (1.9%) from cord compression. Other diagnoses include; acute motor axonal neuropathy 3 (2.8%), acute disseminated encephalomyelitis 2 (1.9%), meningoencephalitis 2 (1.9%), diabetic polyneuropathy 2 (1.9%), and chemotherapy-induced neuropathy 1 (0.9%). Most cases, 42/106 (39.6%) were admitted during the spring season. Conclusion: GBS was the most common cause of AFP in all age groups. Most of the AFP cases occurred during the spring season. No case of poliomyelitis was found.

Sjögren syndrome is an autoimmune disorder characterized by lymphocytic infiltration of exocrine gland. The most common symptom by virtue of its involvement includes dryness of eyes, mouth, and parotid gland enlargement. However, the disease may be associated with extraglandular manifestation affecting multiple organs. Such a presentation involves renal involvement with tubular dysfunction manifesting as severe hypokalemia.

Abstract: Quadriparesis after intramuscular trigger point injections for myofascial pain syndrome has been rarely reported in the literature. A 37-year-old male patient presented with myofascial pain syndrome and was given trigger point injections in trapezius muscles under ultrasound guidance. The patient noticed weakness in all the 4 limbs at approximately 12 hours after the procedure, which gradually progressed to functional quadriplegia at the time of presentation to the emergency department. On examination, he had quadriparesis with no sensory involvement and superficial reflexes were normal. MRI screening of the whole spine was unremarkable, and MRI brain suggested an incidental granuloma, which could not explain his symptoms. Blood tests revealed severe hypokalemia (2.2 mEq/L) and deranged thyroid function tests. Immediate potassium correction with intravenous and oral potassium chloride was initiated, and the patient showed improvement within 6 hours of initiating correction. Stress of the procedure, use of steroids with mineralocorticoid effects such as methylprednisolone, or deranged thyroid function tests may have acted as triggers to precipitate hypokalemic paralysis in the patient. Knowledge of this complication is essential as prompt diagnosis and timely management of hypokalemia can result in complete resolution of the symptoms. [ABSTRACT FROM AUTHOR]

Hypokalemic periodic paralysis (HPP) is a rare heterogenous neuromuscular disorder presenting with acute weakness. Though most cases are known to be familial or primary there are other underlying secondary causes which require evaluation and if not corrected could lead to recurrent episodes.Distal renal tubular acidosis (RTA) is one such association which has been described. Type 1/Distal RTA is known to cause renal potassium wasting thereby leading to hypokalemia. Patients with Distal RT A are unable to acidify their urine. The causes of Distal RTA can be hereditary, congenital, acquired or idiopathic. Severe hypokalemia with RTA has been described along with Medullary sponge Kidney and other cystic lesions in the kidney. There have been previous reports of hypokalemic paralysis occurring secondary to RT A precipitated by cystic kidney disease. We hereby report one such of hypokalemic periodic paralysis secondary to distal RTA which was associated with cystic kidney disease.

Background and Aims: As a part of the Global Polio Eradication program by the World Health Organization (WHO, 1988), surveillance of acute flaccid paralysis (AFP) was an important public health activity in many countries. With nearing eradication of poliomyelitis, other causes of AFP are gaining importance in both children and adults. Our study was designed to know the clinical characteristics and differential diagnosis of causes of AFP, including distribution by age, gender, and time. This was a prospective observational study. Methods: AFP cases were diagnosed on history and physical examination. The underlying etiology was ascertained by appropriate laboratory investigations such as arterial blood gas analysis, urinary pH, electrolytes, thyroid profile, electrophysiological studies, cerebrospinal fluid (CSF) analysis, and imaging. Results: Between July 2010 and September 2012, 106 cases of AFP were enrolled in the study. The mean age of males was 40.2 years (standard deviation [SD] 17.1) and the mean age of females was 33.4 years (SD 14.1). Of 106 patients, 61 (57.5%) were male and 45 (42.5%) were female. Out of 106 patients, 58 (54.7%) were suffering from Guillain-Barre′ syndrome (GBS), 15 (14.2%) from hypokalemic paralysis, 8 (7.5%) from myasthenia gravis, 8 (7.5%) from thiamine deficiency, 5 (4.7%) from transverse myelitis, and 2 (1.9%) from cord compression. Other diagnoses include acute motor axonal neuropathy 3 (2.8%), acute disseminated encephalomyelitis 2 (1.9%), meningoencephalitis 2 (1.9%), diabetic polyneuropathy 2 (1.9%), and chemotherapy-induced neuropathy 1 (0.9%). Of 106 patients, 42 (39.6%) were admitted during the spring season. Conclusion: GBS was the most common cause of AFP in all age groups. Most AFP cases occurred during the spring season. No case of poliomyelitis was found.

Sjogren syndrome (SS) is a systemic autoimmune disorder with predominant exocrine gland involvement leading to sicca symptoms. Among extraglandular manifestations, renal disease is the most common. Tubular interstitial nephritis and renal tubular acidosis (RTA) are the common presentations. Mild hypokalemia associated with distal RTA is common in SS, however, severe hypokalemia causing paralysis is unusual. We report the case of a 26-year-old female who presented with hypokalemic paralysis. On evaluation, distal RTA was diagnosed. Further evaluation showed positive SS-a/SS-b antibodies in high titer, which confirms the diagnosis of primary SS. Our report illustrates that SS is a rare but important cause of hypokalemic paralysis. [ABSTRACT FROM AUTHOR]

The objective of the study is to prospectively evaluate the spectrum of clinical and subclinical renal involvement in patients with primary Sjogren’s syndrome (pSS). Of the 174 patients screened, seventy patients with pSS underwent renal function tests, urine examination, renal ultrasound, arterial blood gases, urine pH followed by urine acidification test and renal biopsy (if indicated). Renal tubular acidosis (RTA) was treated with alkali replacement and moderate-severe tubulointerstitial nephritis (TIN) was treated with oral prednisolone. Sixty-two patients completed 1-year follow-up. A comparison was made between patients with and without renal involvement. Thirty-five (50%) patients had renal involvement. They had a lower baseline eGFR (71.85 ± 18.04 vs. 83.8 ± 17, p = 0.005). Twenty-nine patients had RTA (25 complete and 4 incomplete). Eleven patients had urinary abnormalities. Patients with RTA (n = 29) were younger (34.9 ± 9 vs. 42 ± 11.3, p = 0.006), had fewer articular (34% vs. 78%, p = 0.001) and ocular sicca (62% vs. 88%, P = 0.01) than those without RTA (n = 41) and commonly presented with hypokalemic paralysis. On biopsy, TIN (9/17) and IgA nephropathy (3/17) were most common. On follow-up, there was no clinically significant change in eGFR; however, one patient with renal calculi and incomplete distal renal tubular acidosis (dRTA) progressed to complete dRTA. Two patients treated with steroids had marginal improvement in eGFR. Renal involvement in pSS is under-recognized with the most common manifestation being RTA presenting with hypokalemic paralysis. These patients are younger with less articular and sicca symptoms. Subclinical RTA may progress to complete RTA. Renal biopsy should be considered in all patients with renal involvement. [ABSTRACT FROM AUTHOR]

Introduction: Hypokalemia is associated with increased morbidity and at times mortality. "Hypokalemic paralysis", particularly if recurrent, has often been considered synonymous with "hypokalemic periodic paralysis (HPP)"; however, diseases such as Gitelman syndrome (GS), Bartter syndrome (BS), and renal tubular acidosis (RTA) can have identical presentation. We have tried to explore the etiological spectrum along with epidemiological and certain clinical, biochemical, and electrophysiological features in patients with hypokalemic paralysis. Materials and Methods: In this observational study, 200 appropriate patients with hypokalemic paralysis (serum K+ <3.5 mmol/L) were evaluated for transcellular shift, extra-renal or renal loss of K+ as the underlying etiology of hypokalemia. We took urinary potassium >25 mmol/day as the cutoff for inappropriate renal loss of potassium in presence of hypokalemia. Serum and urinary osmolality along with arterial blood gas analysis were performed in all patients with renal loss of potassium. Serum and urinary sodium, potassium, calcium, magnesium, chloride, and creatinine were measured in normotensive patients with metabolic alkalosis. Hypertensive patients were evaluated with plasma aldosterone and renin activity. Results: Probable GS topped the list involving 28% individuals of the entire cohort while probable BS, distal RTA, and HPP were diagnosed in 20%, 22%, and 19% cases, respectively. Rural tribal population (61%) and age group of 30-40 years suffered the most (48%) with concentration of cases in hot and humid summer months. Conclusions: We suggest that patients with hypokalemic paresis should be evaluated thoroughly to unmask the underlying etiology that may have a different therapeutic and prognostic connotations and not to use the term "periodic" in cases of recurrent hypokalemic paralysis. [ABSTRACT FROM AUTHOR]

Hypothyroidism and distal renal tubular acidosis causing hypokalemic paralysis (HP) have been described only in four female patients. HP as the initial manifestation of uncomplicated diabetes has been reported only in three young males. We report two middle-aged patients presenting with gradual-onset areflexic quadriparesis and neck flop, associated with urinary potassium losses, and recovering over 3 days. The male patient with alcohol abuse had urine pH >5.5 and hyperchloremic metabolic acidosis due to renal tubular acidosis and hypothyroidism. The second, a hypertensive female, had metabolic alkalosis, hypomagnesemia, and diabetes mellitus diagnosed at admission. Both these patients improved with intravenous and oral potassium supplementation.

Acute hypokalemic paralysis is a relatively rare cause of acute weakness. It may resolve spontaneously; however, it may be a potential life-threatening condition. Hypertension may be considered the most important finding in combination with hypokalemic paralysis for raising the suspicion of primary hyperaldosteronism (PHA). A 55-year-old hypertensive Mexican woman was admitted to the Emergency Unit with a sudden onset of generalized paralysis. An endocrinological workup and an abdominal magnetic resonance imaging revealed PHA with a 1.5 cm left adrenal tumor. After preoperative medication, left adrenalectomy was performed with single-incision laparoscopic surgery (SILS). The duration of the surgery was 45 min, and no postoperative complication was encountered. The patient was discharged after 24 h. Hypokalemic paralysis may be due to different conditions, but it may raise the suspicion of PHA in combination with a history of generally mild hypertension. Laparoscopic adrenalectomy is the preferred operation for unilateral adrenal adenomas that cause PHA. Single-incision laparoscopic surgery is a step-forward technique that improves the cosmesis, decreases access-related morbidity, and increases the postoperative recovery. We report a case with acute hypokalemic paralysis due to PHA and treated with SILS. [ABSTRACT FROM AUTHOR]

Key Clinical Message In rare cases, patients with Gitelman syndrome may present with hypokalemic paralysis mimicking Guillain-Barré syndrome. The severity of resultant symptoms may be life-threatening. Controversial drugs such as aldactone, amiloride, and eplerenone should be used in this situation despite the lack of safety data. [ABSTRACT FROM AUTHOR]

With an ever-increasing trend in the side effects of antiretroviral therapy (ART), usage of new regimens to decrease the mortality and morbidity has come into picture. Here we report a case of tenofovir-induced hypokalemic paralysis. A 60-year-old female patient came to a medical outpatient department with quadriparesis. History revealed that she was diagnosed with HIV 6 years back and was on zidovudine, lamivudine, and efavirenz. Three months later, she developed severe anemia because of which zidovudine was replaced by tenofovir. On evaluation, there was hypokalemia with appropriate electrocardiography changes. As previous literature showed association of hypokalemia with tenofovir, we attributed this finding to the usage of tenofovir. ART was stopped, and the patient was given potassium supplements and potassium-rich diet. There was dramatic improvement with the treatment and the patient regained muscle strength. After 1 week, she was put on other alternative regimen consisting of abacavir, lamivudine, and efavirenz. Her CD4 count was improved without any complaints. The patient was monitored on outpatient basis in ART center. [ABSTRACT FROM AUTHOR]

Background: Hypokalemic paralysis is characterized by episodes of acute muscle weakness associated with hypokalemia. In this study, we evaluated the possible etiological factors in patients of hypokalemic paralysis. Materials and Methods: We reviewed the records of 29 patients who were admitted with a diagnosis of hypokalemic paralysis. Modified Guillain-Barre΄ Syndrome disability scale was used to grade the disability. Results: In this study, 15 (51.7%) patients had secondary causes of hypokalemic paralysis and 14 patients (42.3%) had idiopathic hypokalemic paralysis. Thyrotoxicosis was present in six patients (20.6%), dengue infection in four patients (13.7%), distal renal tubular acidosis in three patients (10.3%), Gitelman syndrome in one patient (3.4%), and Conn′s syndrome in one patient (3.4%). Preceding history of fever and rapid recovery was seen in dengue infection-induced hypokalemic paralysis. Approximately 62% patients had elevated serum creatinine phosphokinase. All patients had recovered completely following potassium supplementation. Patients with secondary causes were older in age, had significantly more disability, lower serum potassium levels, and took longer time to recover. Conclusion: In conclusion, more than half of patients had secondary causes responsible for hypokalemic paralysis. Dengue virus infection was the second leading cause of hypokalemic paralysis, after thyrotoxicosis. Presence of severe disability, severe hypokalemia, and a late disease onset suggested secondary hypokalemic paralysis.

Renal tubular acidosis (RTA) is a constellation of syndromes arising from different derangements of tubular acid transport. Recent advances in the biology of urinary acidification have allowed us to discern various molecular mechanisms responsible for these syndromes. RTA often presents as renal stone disease with nephrocalcinosis, ricket/osteomalacia and growth retardation in children with ultimate short stature in adulthood. The case reported here has features of distal renal tubular acidosis (dRTA), hypokalemic paralysis, primary hypothyroidism, growth retardation, osteomalacia and osteopenia leading to stress fracture. All these features presenting in a single case (as in our case) is a rare occurrence, so far other cases of distal renal tubular acidosis (dRTA) have been reported.

Introduction: Dengue, an acute viral disease transmitted by Aedes mosquitoes, is highly endemic in many tropical and subtropical areas of the world. Neurological complications of dengue infection have been observed more frequently in the recent past and some studies highlighted varied neurological complications arising in the course of dengue illness. In this retrospective study, we report various neurological complications observed during the last 2 years in patients of dengue fever. Materials and Methods: The patients presenting with neurological complications with positive serology (IgM antibody) for dengue infection were consecutively recruited from the Department of Neurology/Medicine from a tertiary center of Lucknow, India. These patients were subjected to a detailed clinical evaluation, laboratory assessment including blood count, hematocrit, coagulation parameters, biochemical assays, serology for dengue fever, enzyme-linked immunosorbent assay for human immunodeficiency virus and other relevant investigations. Results: Twenty-six patients with neurological complications associated with confirmed dengue infection were observed during the last 2 years. Eighteen of these patients were male. Of the 26 patients, 10 patients were suffering from brachial neuritis, four patients had encephalopathy, three patients were consistent with the diagnosis of Guillain Barre syndrome, three patients had hypokalemic paralysis associated with dengue fever and two patients had acute viral myositis. Opsoclonus-myoclonus syndrome was diagnosed in two patients, myelitis in one patient and acute disseminated encephalo-myelitis also in one patient. Conclusion: Dengue fever was associated with widespread neurological complications. Brachial neuritis and opsoclonus-myoclonus syndrome were observed for the first time in this study.

The article presents a case study of a 33-year-old woman with tetraparesis who was taken to the emergency room because of progressive weakening in all four extremities. The article presents differential diagnosis including polymyositis, acute intermittent porphyria, and polyneuropathy due to thiamine deficiency.

Sjögren′s syndrome (SS) is a chronic autoimmune disease, chiefly affecting the exocrine glandular function of salivary glands and lacrimal glands. Rarely, it involves the kidneys, central and peripheral nervous system, muscloskeletal apparatus and lungs. We report a rare constellation of SS with distal renal tubular acidosis and quadriparaesis in a young female. History of quadriparaesis was acute, with rapid progression. Supplementary treatment for severe hypokalemia was instituted at the earliest, lest the patient develop respiratory muscle weakness. Concomitantly, metabolic acidosis with alkaline urine was suspected and subsequently investigated. Eventually, this was attributed to impaired renal acidification of urine in the distal tubules. History of dryness of eyes and mouth since 6 months justified salivary gland biopsy. The results yielded a lymphocytic infiltrative pathology strongly favoring SS. The patient benefited from prompt potassium replacement therapy and had complete resolution over the next week. Supportive treatment for predictable manifestations was continued along with potassium supplements.

Sjögren syndrome is an autoimmune disorder characterized by lymphocytic infiltration of exocrine gland. The most common symptom by virtue of its involvement includes dryness of eyes, mouth, and parotid gland enlargement. However, the disease may be associated with extraglandular manifestation affecting multiple organs. Such a presentation involves renal involvement with tubular dysfunction manifesting as severe hypokalemia. [ABSTRACT FROM AUTHOR]

Primary Sjögren′s syndrome (pSS) is a chronic autoimmune disease characterized by a progressive lymphocytic infiltration of the exocrine glands with varying degrees of systemic involvement. Overt or latent renal tubular acidosis (RTA), caused by tubulointerstitial nephropathy, is a common extraglandular manifestation of pSS. Hypokalemic paralysis is a well known, albeit rare complication of severe distal RTA from any cause. Cases of pSS manifesting for the first time as hypokalemic paralysis caused by distal RTA have been rarely reported. We herein present our experience of two cases, who presented to us for evaluation of hypokalemic paralysis and on work up found evidence of distal RTA, which on further work up found to be secondary to pSS. A high index of suspicion for pSS should be kept in all patients with hypokalemic paralysis.

Hypokalemic disease is a disorder in which the amount of serum’ s potassium declines and the patient faces limbs weakness. In this disease, eye muscle and respiratory muscles rarely become involved and death may follow due to respiratory paralysis and heart conducting disturbances. Since this disease is treatable and progressive weakness can be prevented, therefore in the study conducted we attempted to compare between the causes and epidemiological characteristics and start of clinical manifestation and the characteristics of this diseases with what had been presented in classical text and foreign sources in order to take effective measure for timely diagnosis. This was a descriptive prospective study. The records of hypocalemically paralyzed patients hospitalized in shahid Beheshti Hospital of Kashan during 1990 to 2000 were used to collect the data such as general condition of the patient, systematic and neurologic examination, serum potasium level, ABG, and paramedical measures like ECG were extracted and used for analysis. 27 patients were identified as Hypokalemic afflicted to paralysis and all were sporadic cases. The starting age for weakness attack was mostly in the second to fourth decade of life. The mean age for attack was 29 years . 96.3 percent were male and the rest were female. The level of potasium in serum of these patients during the weakness attack was mostly within 1 to 3.5 meq/L and the most changes in ECG was related to decrease in height at T and appearance of U- waves. 11 patients have more than 3 attacks (40.7 percent ), 10 patients faced all-attacks (37.3 percent) and 6 patients experienced 2 times attack (22 percent).Considering that hypokalemic paralysis disorder is a treatable disease and immediate diagnosis and treatment reduces cardiac and muscular problems, it is necessary for the physican who treat patients referring with flaccid paralysis to keep in mind four limbs of this disease and use diagnostic measures.

We present a middle-aged woman with a prior history of central nervous system (CNS) demyelinating disorder who presented with an acute onset quadriparesis and respiratory failure. The evaluation revealed distal renal tubular acidosis with hypokalemia and medullary nephrocalcinosis. Weakness persisted despite potassium correction, and ongoing evaluation confi rmed recurrent CNS and long-segment spinal cord demyelination with anti-aquaporin-4 antibodies. There was no history of dry eyes or dry mouth. Anti-Sjogren's syndrome A antigen antibodies were elevated, and there was reduced salivary fl ow on scintigraphy. Coexistent antiphospholipid antibody syndrome with inferior vena cava thrombosis was also found on evaluation. The index patient highlights several rare manifestations of primary Sjogren's syndrome (pSS) as the presenting features and highlights the differential diagnosis of the clinical syndromes in which pSS should be considered in the Intensive Care Unit. [ABSTRACT FROM AUTHOR]

Dengue is associated with many neurological dysfunctions. Up to 4% of dengue patients may develop neuromuscular complications. Muscle involvement can manifest with myalgias, myositis, rhabdomyolysis and hypokalemic paralysis. Diffuse myalgia is the most characteristic neurological symptom of dengue fever. Dengue-associated myositis can be of varying severity ranging from self-limiting muscle involvement to severe dengue myositis. Dengue-associated hypokalemic paralysis often has a rapidly evolving course; benign nature; excellent response to potassium; and, often leads to diagnostic confusion with other dengue-associated neuromuscular disorders. Rhabdomyolysis is the most severe form of muscle involvement and may be life-threatening. Guillain-Barré syndrome is another frequent neuromuscular dengue-associated complication. Dengue-associated Guillain-Barré syndrome responds very well to intravenous immunoglobulins. Predominant spinal gray matter involvement has been reported in a patient presenting with areflexic paraparesis. Mononeuropathies often manifest with paralysis of the diaphragm due to phrenic nerve dysfunction. Brachial plexopathy, in the form of neuralgic amyotrophy, has been described much more frequently than lumbo-sacral plexopathy. Early recognition of these neuromuscular complications is needed for successful treatment and to prevent further disabilities. [ABSTRACT FROM AUTHOR]