Intravenous Potassium Replacement Research Articles

FRI512 Thyrotoxic Periodic Paralysis With Extreme Hypokalemia Precipitated By Acute Alcohol Intoxication In A Patient With Graves’ Disease

Abstract Disclosure: J. Batra: None. A.R. Ankireddypalli: None. J. Kaur: None. Introduction: Thyrotoxic periodic paralysis (TPP) is a muscle and electrolyte disorder, mostly seen in the setting of hyperthyroidism. It is characterized by reversible painless muscle weakness and hypokalemia. Prevalence is highest in East Asian populations, approximately 2%, and 0.1-0.2% in other populations. Males are much more likely to be affected. Common provoking factors include exercise, fasting, and changes in diet. Clinical case: A 29-year-old male of East Asian ethnicity presented to the hospital with the complaint of multiple bouts of inability to lift his extremities for 1 day. He also complained of generalized weakness. He did not have any changes in his mental status and was fully oriented at the time of the presentation. No breathing difficulty was reported. He had been drinking the night before with his friends and drank 1 L of vodka. His past medical history was significant for hyperthyroidism secondary to Graves’ disease, which was diagnosed a year ago. He had been prescribed methimazole but had not been adherent to the medication. The basic metabolic panel revealed undetectable serum potassium of <1.5 (3.4 to 5.3 mmol/L). The rest of the electrolytes and renal function were unremarkable. TSH was suppressed at <0.01 (0.3 to 4.20 uIU/L) and free T4 levels were significantly elevated at 7.77 (0.9 to 1.70 ng/dL). The thyrotropin receptor antibody was 33 (0.00 to 1.75 IU/L). EKG showed sinus tachycardia with nonspecific T-wave abnormalities. Thyroid ultrasound showed diffusely heterogenous parenchyma with diffusely increased blood flow throughout the thyroid on doppler. Echocardiogram showed a normal ejection fraction of 55-60% with mild concentric left ventricular wall thickening consistent with left ventricular hypertrophy. He was initially treated with intravenous potassium replacement and high doses of propylthiouracil, hydrocortisone, and propranolol, leading to the resolution of his symptoms. He was discharged on methimazole and propranolol therapies. Learning points: • Patients with Graves’ disease are routinely counseled against tobacco use to avoid worsening of orbitopathy. Hyperthyroid patients should also be counseled regarding avoidance or moderation of alcohol intake to avoid this rare but potentially life-threatening complication of thyrotoxic periodic paralysis. • The incidence of TPP is significantly higher in the East Asian populations, especially among males (8.7-13%). Counseling regarding provoking factors, the importance of adherence to medications, and the maintenance of euthyroidism to avoid TPP is essential. Presentation: Friday, June 16, 2023

Hypokalemic Periodic Paralysis: A Case Report

Introduction: Hypokalemic Periodic Paralysis is one form of Periodic Paralysis, a rare group of disorders that can cause sudden onset weakness. Although rare, Periodic paralysis must be differentiated from other causes of weakness and paralysis so that the proper treatment can be initiated quickly. Case Report: A 72 year-old elderly male presented to the emergency room with sudden onset of paralysis. He had no respiratory or swallowing difficulty and was able to move his neck and facial muscles. Neurologic exam revealed flaccid paralysis bilateral lower extremities which involved the proximal and distal muscles. Sensation was intact but deep tendon reflexes were slightly diminished to 3 out of 4 throughout. RFT deranged with serum creatinine level of 1.7 (0.6- 1.2mg/dl), potassium level of 1.6 (3.5–5 mmol/L), magnesium level of 0.9 (1.3-2.1meq/l). Electrocardiogram revealed bradycardia and left axis deviation. Two hours after initiation of intravenous potassium replacement, the patient's neurologic symptoms started resolving. The patient was diagnosed with Hypokalemic Periodic Paralysis and was started on calcium channel blocker for control of blood pressure. He was discharged home with an appointment to follow up. Conclusion: Periodic Paralysis should be kept in mind when a patient comes with sudden onset weakness or paralysis, especially when other diseases have been ruled out. It can be life threatening if the treatment is improper, but intervention and subsequent correction of potassium abnormalities can clear the symptoms completely. The underlying etiology should be searched properly to avoid recurrence or persistence of the paralysis.

ODP442 Posaconazole-induced Pseudohyperaldosteronism (PIPH) in Patient Treated for Acute Myeloid Leukemia

Abstract Case summary A 62-year-old Caucasian female presented to our institute with mechanical fall complicated by cervical spine fracture. She had known history of essential hypertension and recently diagnosed acute myeloid leukemia with myelodysplasia related changes (AML-MRC). She had undergone induction chemotherapy with combination of daunorubicin and cytarabine, resulting in chemotherapy induced prolonged pancytopenia. She was initially started on primary prophylaxis with fluconazole, but was switched to voriconazole due to persistent neutropenia. Patient then developed bilateral upper and lower extremity erythematous popular rash on voriconazole. Decision at that time was to switch to Posaconazole 300 mg orally daily. Three months after initiating Posaconazole, patient presented with severe hypokalemia (2.1 mmol/L) and hypertension. Previously her blood pressure was under control with amlodipine, lisinopril and nadolol. Hypokalemia persisted despite aggressive oral and intermittent intravenous potassium replacement therapy. No sources of potassium loss were identified on clinical history. She had persistently elevated blood pressure (systolic blood pressure of 150-180 mmHg) despite being on her home anti-hypertensive regimen. Further work up showed undetectable plasma aldosterone of less than 1 ng/dL (normal < 28 ng/dL) and plasma renin activity level was suppressed to 0.14 ng/mL/h (normal 0.25–5.82 ng/mL/h) with concurrent potassium of 2.9 mmol/L (normal 3.5-5.3 mmol/l). Diagnosis of pseudohyperaldosteronism was made at this time. Posaconazole gradually stopped and eplerenone 25 mg daily was commenced to selectively block mineralocorticoids receptors to control blood pressure. Subsequently hypokalemia resolved after stopping posaconazole and blood pressure normalized with her original home anti-hypertensive regimen. Eplerenone was eventually stopped. Her potassium level and blood pressure remained normal 2 weeks after discharge. Discussion Recent studies have shown the presentation of hypokalemia and hypertension in nearly a quarter of patients on Posaconazole. The clinical presentation of hypokalemia and hypertension with apparent mineralocorticoid excess was evident in our patient and was consistent with posaconazole-induced pseudohyperaldosteronism (PIPH). Posaconazole interference with the steroid synthesis pathway has been described in various literature. Both cortisol and aldosterone activate aldosterone receptors. In the case of posaconazole, excess mineralocorticoid effect is due to relative selectivity of posaconazole for 11ΒHSD2 inhibition. 11ΒHSD2 inhibition causes increased serum cortisol level by preventing the conversion to inactive cortisone. The high cortisol level cross-reacts with the mineralocorticoid receptor leading to apparent mineralocorticoid excess with low serum aldosterone level and low plasma renin activity. The degree of pseudohyperaldosterone effect on systolic blood pressure and hypokalemia has been strongly associated with serum posaconazole level in some studies. Our patient had resolution of uncontrolled hypertension and hypokalemia after withholding the posaconazole and short term treatment with selective mineralocorticoid receptor blocker. Conclusion Early diagnosis and to allow for early intervention with cessation of the offending agent or treatment with mineralocorticoid antagonists, such as spironolactone and eplerenone is necessary in PIPH. Presentation: No date and time listed

PMON285 Hypokalemic Periodic Paralysis: A Rare Presentation of Primary Hyperaldosteronism

Abstract Background Primary hyperaldosteronism (PHA) is caused by excessive production of aldosterone from the adrenal glands. Aldosterone levels are usually independent of renin, angiotensin II or sodium status, and often result in hypertension (HTN), hypokalemia and metabolic alkalosis. The most common presentation of this condition is with asymptomatic mild to severe or refractory HTN. This case highlights a patient presenting with hypokalemic periodic paralysis as the first sign of PHA. Clinical Case A 35 year old previously healthy Chinese male, presented with sudden onset bilateral lower extremity weakness for 1 day. This was associated with mild transient lower back pain and fatigue. He had no history of trauma, recent travel, exposure to animal or tick bites. He reported no recent illness or vaccination. His family history was negative for hypertension and various endocrinopathies. The patient was not on any medications and did not consume licorice. His exam was significant for a blood pressure (BP) of 217/136 mmHg, with lower limb evaluation revealing power of 3/5, normal reflexes and a positive heel to shin test. He demonstrated an unsteady gait but Romberg's sign was negative. Upper limb exam was normal. Laboratory findings were remarkable for potassium 1.9 mmol/L, bicarbonate (CO2) 37 mmol/L, normal magnesium (Mg), normal TSH and blood gas showing metabolic alkalosis. Subsequent testing showed renin 0.35 ng/ml/hr, aldosterone 23 ng/dl and aldosterone/pra ratio 66. Saline infusion test confirmed the diagnosis of PHA. Other endocrinologic tests were normal. Electrocardiogram showed prolonged QT interval and U waves. Renal ultrasound was negative for renal artery stenosis and CT abdomen/pelvis showed a 2.4 cm left adrenal adenoma. The patient was admitted to the intensive care unit for 24 hours, where he received intravenous potassium replacement and was started on spironolactone and other antihypertensive medications, which he was discharged on, along with oral potassium. His symptoms resolved after potassium levels normalized and he subsequently had a left adrenalectomy. Conclusion With PHA being the most common endocrinological cause of HTN, clinicians should recognize indicators of underlying PHA even in rare presentations such as this. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

Distal renal tubular acidosis presenting with an acute hypokalemic paralysis in an older child with severe vesicoureteral reflux and syringomyelia: a case report

BackgroundDistal renal tubular acidosis (dRTA) is the most common type of renal tubular acidosis (RTA) in children. Pediatric dRTA is usually genetic and rarely occurs due to acquired issues such as obstructive uropathies, recurrent urinary tract infections (UTIs), and chronic kidney disease (CKD). Although persistent hypokalemia frequently occurs with dRTA, acute hypokalemic paralysis is not frequently reported, especially in older children.Case presentationAn eight-year-old girl presented with an acute first episode of paralysis. A physical examination revealed normal vital signs, short stature consistent with her genetic potential, and decreased muscle strength of her upper and lower extremities. Preexisting conditions included stage 4 CKD due to recurrent UTIs, severe vesicoureteral reflux and bilateral hydronephrosis, neurogenic bladder, and multisegment thoracic syringomyelia. Her laboratory work-up revealed hypokalemic, hyperchloremic metabolic acidosis with a normal anion gap. She also had a urine osmolal gap of 1.9 mOsmol/kg with a high urine pH. Intravenous potassium replacement resulted in a complete resolution of her paralysis. She was diagnosed with dRTA and discharged with oral bicarbonate and slow-release potassium supplementation.ConclusionsThis case report highlights the importance of considering dRTA in the differential diagnosis of hypokalemic acute paralysis in children. Additionally, in children with neurogenic lower urinary tract dysfunction and recurrent UTIs, early diagnosis of spinal cord etiology is crucial to treat promptly, slow the progression of CKD, and prevent long-term complications such as RTA.

A life-threatening case of pseudo-aldosteronism secondary to excessive liquorice ingestion

BackgroundLiquorice is found in many food products, soft drinks, and herbal medicines. Liquorice ingestion is an uncommon cause of apparent mineralocorticoid excess or pseudo-aldosteronism. The mechanism involves the inhibition of 11-beta-hydroxysteroid dehydrogenase type-2 by the active ingredient called glycyrrhizin. This leads to the uninhibited activation of mineralocorticoid receptors by cortisol. Confectionary products that contain liquorice are readily available in many countries around the world.Case presentationWe report a case of severe refractory hypokalaemia with hypertensive crisis and acute pulmonary oedema due to excessive liquorice consumption. A 79-year-old female presented to the emergency department following a road traffic accident. She described feeling weak and dizzy while driving before the collision. She attended her general practitioner (GP) several weeks earlier for fatigue and was being managed for hypokalaemia on oral potassium supplements. Investigations revealed hypertension (BP 180/69 mmHg), severe hypokalaemia (K 2.2 mmol/l), normal renal function, normal serum magnesium with metabolic alkalosis. Spot urinary potassium was 22 mmol/l. The patient denied taking medications including over-the-counter or herbal medication that can cause hypokalaemia. Hypokalaemia persisted despite aggressive intravenous (i.v.) and oral potassium replacement. She later developed a hypertensive crisis (BP 239/114 mmHg) with pulmonary oedema. She required admission to the intensive care unit and was managed with intravenous furosemide infusion and isosorbide dinitrate infusion. On further discussion, our patient admitted to struggling with nicotine cravings since quitting smoking two months earlier. She began eating an excessive amount of liquorice sweets to manage her cravings. Suppression of plasma renin and aldosterone supported the diagnosis of apparent mineralocorticoid excess secondary to excessive liquorice consumption. Her symptoms and hypokalaemia resolved after stopping liquorice intake.ConclusionsThis case highlights the life-threatening and refractory nature of hypokalaemia secondary to excessive liquorice consumption. This case also emphasizes the importance of comprehensive history taking including dietary habits. Increased awareness among the public is required regarding the potential health hazards of excessive liquorice consumption.

Caffeine-induced hypokalemia: a case report

BackgroundWith an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. However, the consumption of massive amounts of caffeine can lead to severe hypokalemia.Case presentationA 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. Laboratory tests revealed low serum potassium concentration (2.6–2.9 mmol/L) and low urine osmolality (100–130 mOsm/kgH2O) in three such prior episodes. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. The patient was not under medication with laxatives, diuretics, or herbal remedies. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized.ConclusionsAn increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.

Clozapine Induced Insulin Dependence

Background: Antipsychotic medications come with an array of potential side effects in a difficult-to-treat population, particularly if management of other comorbidities is required. A review of the literature shows some studies have discussed the possibility of antipsychotic medication inducing hyperglycemia by blocking pancreatic M3 receptors. Other studies have shown dramatic worsening of metabolic parameters in patients who already have Type 2 Diabetes Mellitus after starting Clozapine. Clinical Case: A 23 year old African American Male with a past history of treatment resistant Schizophrenia presented to the ED with hyperglycemia and altered mental status. Blood sugar 489 mg/dL, anion gap 28 mmol/L, bicarb 13 mmol/L, white Blood Cell count 9.0 x10^3/cmm. Urine positive for Ketones. Chest Xray and EKG were normal, there were no obvious signs of infection. This was the sixth admission for Diabetic Ketoacidosis (DKA) in the past 10 months. Antibodies obtained showed negative Glutamic Acid Decarboxylase Autoantibodies (<5 IU/mL), Islet Cell Antibody IgG, Zinc Transporter 8 Antibody (<10 U/mL), IA-2 (<5.4 U/mL). C-peptide levels were in the low normal range (1.12 ng/mL) with a blood sugar 204 mg/dL. Prior to 10 months ago, the patient did not have a diagnosis of diabetes, with labs showing expected normal fasting blood sugar levels (90s mg/dL) and triglyceride levels of 150 - 200 mg/dL. One month after starting Clozapine for treatment resistant Schizophrenia, A1c doubled to 12.3%, Triglycerides increased to 1,378 mg/dL. The patient had been insulin dependent since the time of starting Clozapine. On this admission, Clozapine was held, DKA resolved with intravenous fluid, potassium replacement, and insulin drip. Repeat testing of c-peptide with blood glucose levels analyzed with the Homeostasis Model Assessment (HOMA) showed increasing HOMA%S (from 93% to 174%) and decreasing HOMA-IR with stopping Clozapine. Psychiatry recommended Clozapine as required treatment of his Schizophrenia, therefore the patient required chronic insulin. Conclusion: This case study shows Clozapine as the only major change in medications or lifestyle in this patient’s case. He demonstrated severe hyperglycemia and development of Diabetes Mellitus within a 4-week period of medication initiation as evidenced by multiple admissions for DKA, with low/normal C-peptide levels and insulin resistance. He has since been managed as a patient with Type 1 Diabetes. Clinicians should take a multidisciplinary approach to clinical surveillance during changes in schizophrenia treatment, particularly with second generation antipsychotics such as Clozapine, with attention to metabolic derangements including DKA.

Effect of Chronic Kidney Disease on Outcomes of Adult Patients Admitted With Hyperosmolar Hyperglycemic State: Analysis of National Inpatient Sample

Background: Treatment guidelines have been well established in patients with HHS and a normal renal function. The mainstay of treatment for patients with HHS includes intravenous volume replacement, potassium replacement, and blood glucose correction by administering insulin. However, this treatment protocol cannot be directly applied to a patient with decreased GFR as it increases the risk of hypoglycemic episodes due to decreased insulin clearance along with increasing the risk of hyperkalemia and volume overload. Hence titrating insulin, maintaining euvolemia and normokalemia becomes further challenging in a patient with HHS in the setting of CKD. Although the above-mentioned complications are well described in multiple studies, there is not enough evidence demonstrating the association between the inpatient mortality and secondary outcomes in patients with HHS with and without CKD.Objective: To compare the inpatient mortality and secondary outcomes in patients admitted with HHS with CKD vs without CKD.Methods: A retrospective cohort study was conducted using the Nationwide Inpatient Sample from 2016 and 2017. About 42 740 hospitalizations who had HHS as primary diagnosis were enrolled and further stratified based on the presence or absence of CKD as a secondary diagnosis using ICD-10 codes. The primary outcome was inpatient mortality and secondary outcomes included length of hospital stay, total Hospital charges, Sepsis, Septic Shock, Acute Kidney Injury (AKI), and Acute Respiratory Failure (ARF). Multivariate regression analysis was done to adjust for confounders.Results: Out of the 42 740 hospitalizations with HHS, about 9 545 had CKD. The in-hospital mortality for patients with HHS was 305 overall, out of which 105 patients had Atrial Fibrillation as a secondary diagnosis. Compared with patients without CKD, patients with CKD had similar in-hospital mortality (aOR 0.93, 95% CI 0.48–1.8, p=0.83) when adjusted for patient and hospital characteristics. Patients with HHS and CKD had similar length of hospital stay, total hospital charges, rate of Sepsis, Septic Shock, and ARF in comparison to patients without CKD; however, patients with CKD had higher odds of developing AKI thorough out hospitalization.Conclusion: This study found that patients admitted with HHS and CKD have similar in-hospital mortality when compared to patients without CKD. However, the study group with CKD has higher odds of developing AKI when compared to the group without CKD. Although AKI is common and correctable in HHS, the above-mentioned association is possible due to the judicious IV fluid replacement in an HHS patient with CKD as a concern for volume overload. Further studies are needed to identify contributing risk factors and establishing fluid replacement guidelines in a patient with HHS and CKD.

Safety of a Nurse-Driven Standardized Potassium Replacement Protocol in Critically Ill Patients With Renal Insufficiency.

In critically ill patients, maintaining appropriate serum potassium concentrations requires careful supplementation to correct hypokalemia but avoid hyperkalemia. At the study institution, an institution-based, nurse-driven standardized electrolyte replacement protocol is used in critically ill patients with a serum creatinine concentration of 2 mg/dL or less. If the serum creatinine concentration is greater than 2 mg/dL, electrolyte replacement requires a physician order. To determine if standardized potassium supplementation is safe in critically ill patients with renal insufficiency not requiring renal replacement therapy. This study was an institutional review board-approved, single-center, retrospective evaluation of critically ill patients receiving intravenous potassium replacement per protocol. Patients were grouped according to serum creatinine concentration (≤ 2 mg/dL or > 2 mg/dL) at the time of replacement. The primary outcome was the incidence of hyperkalemia (potassium concentration ≥ 5 mEq/L) following potassium replacement. Secondary outcomes were the incidence of hyperkalemia, change in serum potassium concentration, and need for hyperkalemia treatment. Outcomes were analyzed using χ2 and t tests. Of 814 patients screened, 145 were included (99 with serum creatinine ≤ 2 mg/dL and 46 with serum creatinine > 2 mg/dL). The incidence of hyperkalemia was not different between groups (P = .57). Five patients experienced hyperkalemia; none received hyperkalemia treatment. Change in serum potassium was similar for patients in the 2 groups (P = .33). A standardized, nurse-driven electrolyte replacement protocol can be used safely in critically ill patients with renal insufficiency not requiring renal replacement therapy.

Short-Lasting Unilateral Neuralgiform Headache Attacks with Conjunctival Injection and Tearing (SUNCT) Status Like Condition: A Rare Case Report and Review of the Literature.

Background: SUNCT (short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing) is rare trigeminal autonomic cephalgia characterized by recurrent, brief, excruciating unilateral, intermittent headache paroxysms over orbital, frontal or temporal region occurring multiple times per day and it can rarely present as “SUNCTstatus like condition” (SSLC). Case Report: A 28-year old male with a history of SUNCT headache for 6 months presented with left forehead stabs lasting for 30 seconds with a frequency of 40-45 episodes per hour for three days followed by infective gastroenteritis. His neurological examination was normal, except left-sided ptosis, tearing, and conjunctival injection. His MRI brain with contrast, MR angiography, and laboratory investigations were unremarkable except mild hypokalemia. He was treated with intravenous fluids, potassium replacement, and high dose methylprednisolone along with an escalated dose of carbamazepine. Review and Conclusion: We have reviewed the previously reported seven cases and our case of SSLC. Female: Male ratio was 3:1and the mean age was 40.87 years. Three patients responded to high dose steroids and three to lignocaine along with rapid escalation or change of anticonvulsant drugs. One case responded to the high dose of lamotrigine, and in a pregnant lady, the pain subsided only after the termination of the pregnancy. One case was secondary to multiple sclerosis, while the rest of seven were primary episodic SSLC. The condition is highly disabling, and the treatment with steroids or lignocaine, along with the rapid escalation of preventive drugs, can provide long-lasting relief

Short-Lasting Unilateral Neuralgiform Headache Attacks with Conjunctival Injection and Tearing (SUNCT) Status Like Condition: A Rare Case Report and Review of the Literature.

Background: SUNCT (short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing) is rare trigeminal autonomic cephalgia characterized by recurrent, brief, excruciating unilateral, intermittent headache paroxysms over orbital, frontal or temporal region occurring multiple times per day and it can rarely present as “SUNCTstatus like condition” (SSLC). Case Report: A 28-year old male with a history of SUNCT headache for 6 months presented with left forehead stabs lasting for 30 seconds with a frequency of 40-45 episodes per hour for three days followed by infective gastroenteritis. His neurological examination was normal, except left-sided ptosis, tearing, and conjunctival injection. His MRI brain with contrast, MR angiography, and laboratory investigations were unremarkable except mild hypokalemia. He was treated with intravenous fluids, potassium replacement, and high dose methylprednisolone along with an escalated dose of carbamazepine. Review and Conclusion: We have reviewed the previously reported seven cases and our case of SSLC. Female: Male ratio was 3:1and the mean age was 40.87 years. Three patients responded to high dose steroids and three to lignocaine along with rapid escalation or change of anticonvulsant drugs. One case responded to the high dose of lamotrigine, and in a pregnant lady, the pain subsided only after the termination of the pregnancy. One case was secondary to multiple sclerosis, while the rest of seven were primary episodic SSLC. The condition is highly disabling, and the treatment with steroids or lignocaine, along with the rapid escalation of preventive drugs, can provide long-lasting relief

Adjuvant chemotherapy-associated febrile neutropenia in a patient with breast malignancy: A case report

Adjuvant chemotherapy has been widely applied in patients with breast malignancy after surgery to prevent its recurrence and to improve survival comprehensively. Febrile neutropenia is one of the most life-threatening chemotherapy-associated toxicities. A 66 years old woman came to an emergency department of a secondary healthcare facility one week after her final chemotherapy with dose regimen of docetaxel and epirubicin, followed by having nausea, vomitus, and general fatigue with a fever of 38.2°C. Based on her medical record, she had experienced breast malignancy for almost two years and had already conducted mastectomy three months after her diagnosis. Her leukocyte number was only 300 cells per mm3, with 23% neutrophil, hypoalbuminemia, and hypokalaemia. She was then treated in an internal ward and was given intravenous ceftazidime, fluid, granulocyte colony-stimulating factor, albumin transfusion, intravenous potassium replacement, and symptomatic medication. After two days of inpatient care, she was referred to an oncology team in a tertiary healthcare facility. Febrile neutropenia is considered as a fever with a low neutrophil number as a result of bone marrow suppression. The neutrophil plays an essential role as the body’s first line of defence. This condition could make the patient more vulnerable to infections. The Patient was given broad-spectrum antibiotics and typically hospitalized to allow close monitoring until the neutropenia was resolved. Febrile neutropenia possesses a serious threat to patients with breast malignancy who are on cytotoxic chemotherapy. Urgent full blood count and immediate broad-spectrum antibiotic administration are significant to reduce morbidity and mortality.

Acquired Long QT Syndrome: A Review of the Literature

The QT interval represents the duration of ventricular depolarization and repolarization. It is measured from the beginning of the QRS complex to the end of the T wave. Prolongation of the QT interval may be congenital or acquired. This increases the risk of polymorphic ventricular tachycardia (i.e torsades de pointes) and cardiac arrest. To increase the awareness of this life-threatening phenomenon I outline an illustrative case in which acquired prolongation of the QT interval due to electrolyte derangement and administration of ciprofloxacin resulted in cardiac arrest due to torsade de pointes. Management of a patient with a long QT syndrome includes Immediate cessation of drugs that prolong the QT interval; cardiac monitoring, serial 12 lead ECGs and transthoracic echocardiography; measurement of serum electrolytes; intravenous potassium replacement; intravenous magnesium replacement; beta-blockade. Causes of acquired prolongation of the QT interval are common in critically ill patients. It is important to recognize this and consider screening with 12 lead ECG to reduce the risk of life-threatening ventricular arrhythmias.

Case report on Southeast Asian ovalocytosis: A patient with type 1 renal tubular acidosis and an asymptomatic patient incidentally found

Two male patients were found to have Southeast Asian ovalocytosis - one incidentally and the other one during the investigations of the aetiology for hypokalemic paralysis. Southeast Asian ovalocytosis is found almost exclusively in Southeast Asia (1, 2). Familial renal tubular acidosis can co-exist with south East Asian ovalocytosis in the same patient (2). Anionexchanger 1 gene AE1 mutation is the underlying pathology and both can originate from the same mutation (2). This can be asymptomatic as in case 1 and can be symptomatic as in case 2. Symptomatic patients need oral potassium and bicarbonate replacement and follow up. After initial clinical assessment and investigations of case 2, he was given intravenous potassium replacement. The correction of metabolic acidosis was made by giving oral sodium bicarbonate 600mg twice daily. Eventually he made full recovery and did not develop further similar episodes.

Acute Neuromuscular Disorders in the Pediatric Intensive Care Unit.

The neuromuscular disorders encountered in the pediatric intensive care unit (PICU) encompass a broad spectrum of pathologies. These include acute disorders (eg, Guillain-Barre syndrome), acute-on-chronic disorders (eg, myasthenia gravis), progressive disorders (eg, muscular dystrophy), and disorders that develop in the PICU (eg, critical illness myopathy/polyneuropathy). Familiarity with the presenting features of these disorders is of paramount importance in facilitating timely diagnosis. We conducted a retrospective review of the medical records of patients admitted to the PICU or Intermediate Care Program (ICP) at a single tertiary children's hospital from 2006 to 2017 with an acute or acute-on-chronic neuromuscular disorder. We did not include patients with a known progressive neuromuscular disorder or critical illness myopathy/polyneuropathy. Twenty-four patients were admitted to the PICU/ICP with acute or acute-on-chronic neuromuscular disorders. Diagnosis and indication for ICU/ICP admission were Guillain-Barre syndrome (n = 6; respiratory failure: 3, respiratory monitoring: 2, autonomic instability: 1), myasthenia gravis (n = 5; airway clearance: 3, respiratory failure: 2), acute flaccid myelitis (n = 3; respiratory failure: 2, respiratory monitoring: 1), periodic paralysis (n = 3; intravenous potassium replacement), rhabdomyolysis (n = 3; monitoring for electrolyte derangements), infant botulism (n = 2; respiratory failure), chronic demyelinating polyneuropathy (n = 1; respiratory failure), and congenital myasthenic syndrome (n = 1; apnea). No patients were admitted to the PICU/ICP with a diagnosis of tick paralysis, acute intermittent porphyria, or inflammatory myopathy. Although acute and acute-on-chronic neuromuscular disorders are encountered relatively rarely in the PICU, familiarity with the presenting features of these disorders is important in facilitating timely diagnosis. This, in turn, enables the institution of effective management strategies, thereby avoiding complications associated with diagnostic delays.

Clinical and Etiological Spectrum of Hypokalemic Periodic Paralysis in a Tertiary Care Hospital in Pakistan.

IntroductionHypokalemic periodic paralysis (HPP) is characterized by muscle weakness secondary to low serum potassium levels. It may be primary in origin or there may be secondary causes like thyrotoxic periodic paralysis, renal or suprarenal causes, or non-renal causes like gastroenteritis.AimTo study the etiology, clinical manifestations, and outcome after therapy of patients with hypokalemic paralysis.MethodologyThe study was conducted from January 2016 to December 2016. Patients fulfilling the diagnostic criteria for hypokalemic paralysis, i.e., flaccid muscle weakness involving two or more limb muscles due to serum potassium < 3.5 mmol/L and with no objective sensory signs were included in the study. Relevant investigations were done. Those with other causes of flaccid weakness or on diuretic therapy were excluded from the study. Data was analyzed using SPSS Version 20.0 (IBM Corp., Armonk, NY).ResultsIn our study, 14 patients out of a total of 18 (14/18, i.e., 77.78%) were male and 4/18 (22.22%) were female [Male: Female ratio: 3.5:1]. The mean age of onset of HPP in males (29.5±10.14 yrs.) was lesser than that of females (41±10.8 yrs.), but this difference was statistically not significant (p<0.066). In the entire sample there were 15/18 cases (83.33%) of primary and 3/18 (16.67%) cases of secondary HPP [2/3 had thyrotoxic periodic paralysis and 1/3 had gastroenteritis]. Furthermore, 12/18 patients (66.66%) had symmetrical weakness (five cases of paraparesis and all were male; seven cases of quadriparesis: six males and one female) and 6/18 (33.33%) had asymmetrical weakness (two paraparesis: one male, one female; four quadriparesis: two males, two females). Statistically, no significant difference (p<0.709) was seen in those with symmetrical versus those with asymmetrical weakness. In this study 7/18 (38.89%) cases had absent, 1/18 (5.55%) had diminished, and 10/18 (55.55%) cases had intact deep tendon reflexes. None of the cases had cranial, bulbar, or respiratory involvement. The mean serum potassium of sample was 3.18±0.5 standard deviation (SD). The reduction in serum potassium was moderate (2.5-3.5 mmol/L) in primary and severe (<2.5 mmol/L) in secondary HPP. Those with quadriparesis had severe hypokalemia with a mean serum potassium of 2.1 mmol/L. Only 3/18 patients had concomitant magnesium deficiency. Patients given intravenous potassium replacement (except one with moderate hypokalemia and given oral replacement) recovered dramatically. The mean recovery time was 38.6±20.3 hours. The recovery time in quadriparesis was about 24 hours and in paraparesis was 12 hours. Only one patient with thyrotoxic periodic paralysis (TPP) and with severe serum potassium deficiency (0.9 meq/L) died due to cardiac arrhythmia. No atypical presentation was seen.ConclusionHPP has male preponderance. The age of onset of HPP is earlier in males than in females. Moreover, males are more prone to have symmetrical weakness. Asymmetrical weakness has almost an equal gender distribution. Primary hypokalemic paralysis is more frequent than secondary. Thyrotoxic periodic paralysis is the commonest cause of secondary periodic paralysis. The recovery time in quadriparesis is almost double the recovery time in paraparesis. Respiratory involvement is rare. HPP is an important differential in the diagnosis of acute flaccid muscle weakness. It should be promptly addressed to prevent recurrence of paralysis.

Hypokalemic Periodic Paralysis With Reversible Electrophysiological Abnormalities: A Case Report

Hypokalemic periodic paralysis (HPP) is a reasonably rare condition, presenting complains being those associated with acute systemic weakness and hypokalemia. Majority of the cases are characterized as familial or primary, whereas sporadic cases are associated with various other conditions such as barium poisoning, hyperthyroidism, renal disorders, endocrinopathies and gastrointestinal potassium losses. We report a unique case in a 5-year-old female child following gastrointestinal losses (vomiting and diarrhea). According to the patient’s mother, for the past 2 days, she was lethargic, unable to walk and hold the neck. She underwent pyelolithotomy for recurrent kidney stones 5 years back. Her neurologic examination revealed diminished bulk overall, decreased tone, power and reflexes in lower limbs with down-going plantars. Labs (except potassium) and electrocardiography were normal. Nerve conduction studies (NCS) favored the diagnosis of Guillain-Barre syndrome. Intravenous immunoglobulin and potassium replacement was started. After a week, patient’s condition had a remarkable improvement. We did a repeat NCS which came out to be normal. Potassium serum values were normal too. We turned back to the other differential diagnosis of HPP. Our case report highlights several important factors. Firstly, it states that the NCS can be deceptive in patients with flaccid paralysis, especially when we are not suspecting hypokalemia. It further explains the importance of suspecting a diagnosis of HPP in a patient presenting with features of Guillain-Barre syndrome following an NCS. J Med Cases. 2018;9(6):177-178 doi: https://doi.org/10.14740/jmc3058w

A case of acute areflexic, flaccid quadriplegia resulting from acute hypophysitis

Introduction: Acute flaccid paralysis, though relatively common, can pose a diagnostic challenge because of its varied etiology. Case Report: We report a 42-year-old Afro-Caribbean woman whose third and final admission over a 3-week period was because of acute onset quadriparesis. At the final admission, she had flaccid paralysis, no ankle and knee reflexes, and equivocal plantar responses. Investigations revealed severe hypokalemia and hypernatremia, increased creatinine, and low adrenocorticotropic hormone, cortisol, follicle-stimulating hormone, luteinizing hormone, and thyroid-stimulating hormone. She had marked polyuria and increased plasma osmolality. Atrial natriuretic factor was detected and chest computed tomography showed a dilated esophagus and bilateral acute pulmonary emboli. Magnetic resonance imaging revealed an enlarged 1.2x1.4x1.8 cm pituitary gland showing enhancement, indicating hypophysitis. She was diagnosed with quadriparesis secondary to hypokalemia and neurogenic diabetes insipidus secondary to panhypopituitarism involving the stalk, which is postulated to have resulted from acute hypophysitis. She made a complete recovery following treatment with intravenous potassium, fluids and hormone replacement. Conclusion: Hypophysitis-induced panhypo-pituitarism with diabetes insipidus remains a rare cause of quadriparesis.

Severe hypokalaemia as a cause of acute transient quadriparesis

Hypokalaemic paralysis covers a heterogeneous group of disorders caused either by an enhanced shift of potassium into the cells or following a significant renal or gastrointestinal loss of potassium. We...