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Abstract Background Primary aldosteronism is characterized by high plasma aldosterone and low renin. The plasma aldosterone-to-renin ratio is recommended for screening. Severe hydronephrosis leads to renal parenchymal ischemia, resulting in increased renin secretion. Since nonsuppression of renin may cause a negative result in the aldosterone-to-renin ratio test, severe hydronephrosis and primary aldosteronism occurring simultaneously in a patient are challenging to diagnose. Case presentation A 54-year-old Chinese man of Han ethnicity was diagnosed with hypertension and severe hypokalemia (minimum 1.57 mmol/L) 13 years prior, and was also diagnosed with severe hydronephrosis due to congenital ureteral stenosis on the left side. His clinical features suggested primary aldosteronism, but the aldosterone-to-renin ratio result of the patient was negative every time he underwent the primary aldosteronism screening test. No further treatment for primary aldosteronism was performed, which led the patient to suffer from severe hypokalemia, such that he was taking 12–15 g/day potassium chloride orally to keep his blood potassium between 3.0 and 3.5 mmol/L (reference value, 3.5–5.5 mmol/L) for 13 years, and the patient needed to be hospitalized in the intensive care unit for rescue several times. At admission, although the aldosterone-to-renin ratio result of the patient was negative, we still did the saline stress test and captopril inhibition test, and the results showed that the plasma aldosterone level was not lower after the test than before the test. Adrenal enhanced computed tomography suggested an adenoma in the left adrenal gland, and the results of adrenal vein sampling suggested that the left side was the dominant side. Therefore, laparoscopic total resection of the left adrenal gland was performed, and 2 weeks later, the patient developed short-term renal function impairment and hyperkalemia, but his renal function and blood potassium returned to normal after treatment that included fluid rehydration. The patient’s biochemical test results and clinical symptoms were completely normal after 1 year. Conclusion We suggest that for patients with a high suspicion of primary aldosteronism in the clinic, comprehensive analysis must be performed in combination with clinical characteristic assessments, such as severe hydronephrosis, if renin is within the normal range or if the aldosterone-to-renin ratio result is negative at screening and diagnostic tests, and adrenal vein sampling should be performed if necessary. It can help avoid misdiagnoses and contribute to the treatment of patients with severe hydronephrosis and primary aldosteronism.

Abstract Background Hypokalemic rhabdomyolysis is a rare clinical manifestation of primary aldosteronism, making its diagnosis challenging, particularly when it becomes the primary presenting symptom. Herein, we present a case of primary aldosteronism with hypokalemic rhabdomyolysis and conduct a related literature review. Case presentation We report the case of a 54-year-old Chinese male patient who presented with intermittent weakness over the past year and was admitted with sudden limb paralysis for 2 days. The final diagnosis was primary aldosteronism accompanied by hypokalemic rhabdomyolysis syndrome. By reviewing the related Chinese and English literature, we noticed that only a few cases were published since 1978. After excluding irrelevant literatures, we summarized and analyzed 43 patients of with primary aldosteronism accompanied by hypokalemic rhabdomyolysis syndrome. All patients showed good recovery, with normalized blood potassium levels, and a majority achieved normalized blood pressure. Some patients still required medication for blood pressure control. Conclusions Primary aldosteronism rarely causes rhabdomyolysis; the occurrence of severe hypokalemia and rhabdomyolysis should prompt consideration of primary aldosteronism in the differential diagnosis. Early detection and treatment are crucial for determining patient prognosis.

Key Clinical Message Several electrocardiographic alterations due to hypokalemia have been described, but the electrocardiographic presentation meeting criteria for occlusion of the left main coronary artery is very rare. We describe a case of hypokalemia simulating it.

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.

We report a case of a young female patient with fatigue, hypokalemia, and hyperglycemia. She had past-history of diabetes mellitus, and was admitted to hospital with a history of fatigue and hypokalemia for 5 years. The patient's examination indicated hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria, and SLC12A3 gene pathogenic mutation. The diagnosis was Gitelman syndrome. Potassium and magnesium supplements were given to improve the patient's fatigue. Serum potassium and magnesium were normal. The blood glucose reached standard after treatment with oral hypoglycemic drugs. This article incorporates literature review to sort out the diagnosis and treatment of Gitelman syndrome, in order to provide feasible reference for clinicians.

Key Clinical Message In managing Sjogren's syndrome, a thorough patient history, proper lab tests, and imaging are crucial. Clinicians should prioritize checking electrolyte levels in cases of muscle weakness, as early detection of hypokalemia can prevent severe complications. Proactive monitoring can avert renal tubular acidosis and improve patient outcomes. Abstract Distal renal tubular acidosis (dRTA) occurs in approximately one‐third of patients with Sjogren's syndrome, a systemic autoimmune disorder characterized by lymphocytic infiltration of exocrine glands, leading to dryness of mucous membranes. Hypokalemic paralysis, a well‐documented but rare complication of dRTA, typically manifests as symmetric proximal muscle weakness of the extremities. We present the case of a 38‐year‐old woman with a history of Sjogren's syndrome diagnosed 3 years prior, who ceased her medication without medical supervision. She presented with quadriplegia, initially beginning unilaterally. This particular presentation is seldom documented in the literature. Laboratory investigations revealed hypokalemia and normal anion gap metabolic acidosis, consistent with dRTA‐induced hypokalemic paralysis. Intravenous potassium chloride was administered, resulting in complete recovery of muscle strength. Hypokalemic paralysis associated with dRTA is typically reversible; however, delays in diagnosis and treatment can lead to life‐threatening complications such as respiratory failure and arrhythmias. Therefore, clinicians should maintain a high index of suspicion for this condition in patients presenting with muscle weakness. Prompt and precise history takingand screening, and initiating appropriate management to prevent adverse outcomes.

Introduction: New-onset Atrial Fibrillation (AF) carries significant morbidity and mortality risk for postoperative patients. Clinical practice guidelines aimed at preventing it are beneficial, with protocols in place to prevent deviations from the standard. Aim: To improve or strengthen the clinical practices that impact the incidence of new-onset AF after off-pump Coronary Artery Bypass Grafting (CABG). Materials and Methods: The present prospective clinical audit was conducted in the Department of Cardiac Anaesthesiology, Bhanubhai Madhuben Patel Cardiac Centre, Bhaikaka University, Anand, Gujarat, India, from January 2021 to June 2021. Study included 50 consecutive patients undergoing off-pump CABG surgery. The monitored standards included the continuation of beta-blocker therapy in the preoperative period, restarting them in the immediate postoperative period, and maintaining serum potassium (S.K+) within the range of 3.5-5.5 mEq/L. The incidence of AF was also noted. The data were analysed using Microsoft Excel. Results: The audit included a total of 50 patients, with 36 males with a mean age of 58.72 years, and 14 females with a mean age of 60.07 years. Preoperative beta-blocker/Calcium Channel Blocker (CCB) therapy on the day of surgery was administered to 45 (90%) patients, while restarting beta-blockers in the immediate postoperative period was done for 49 (98%) patients. S.K+ levels were maintained within the range in 31 (62%) patients. The last standard was reaudited, and compliance was achieved in 39 (78%) patients. New-onset AF occurred in 4 (8%) and 5 (10%) patients in the audit and reaudit samples, respectively. Conclusion: Clinical audit is a process that helps to identify the lacunae in clinical practices that affect patient outcomes. In the current study, clinical audits have aided in measuring compliance with different clinical practices, as per Institutional protocols. They have also assisted in increasing compliance with clinical practices where measured compliance was below the targeted goal.

Inherited salt-wasting tubulopathies include antenatal Bartter syndrome (BS), classical (tip 3) BS, and Gitelman syndrome. BS is an autosomal recessive inherited syndrome associated with impaired sodium and chloride reabsorption in the renal tubule. In classical BS cases with mutations in CLCNKB gene, dehydration episodes are observed within the first year of life. Polyuria, polydipsia, and dehydration are common symptoms in BS. Hypokalemia, hypochloremia, and metabolic alkalosis are observed in almost all of the cases. In this article, we presented a case of type 3 BS without metabolic alkalosis. In the presence of failure to thrive, polyuria, and low sodium, potassium, and chloride, even in the absence of metabolic alkalosis, type 3 BS should be considered in the differential diagnosis.

Objective: To determine the frequency of hypokalemia among COVID-19 patients and assess its impact on the patients management. Study type, settings & duration: It was a cross-sectional study conducted at Mayo Hospital, Lahore from July 2020 to January 2021. Methodology: A total of 212 SARS-COV-2 positive patients who had developed severe disease were enrolled. Based on the level of potassium, the patients were classified as mild, moderate and severe hypokalemia cases. Data was collected using a structured questionnaire including demography, clinical presentations and medication including use of anticoagulant and steroids. Results: Of the total 210, 46 (21.9%) patients had hypokalemia and among them 23 (11%) showed mild, 17 (8.1%) moderate and 6 (2.9%) severe hypokalemia. Out of 210, 17 (23.9%) patients were treated with hydrocortisone, 11 (17.4%) with methylprednisolone and 18 (23.3%) with dexamethasone and no significant difference was seen in development of hypokalemia (p =0.630). Similarly, 39 (21.4%) patients were given enoxaparin and 7 (24.1%) were given heparin, but no significant association was found between the type of anticoagulant being given and hypokalemia (p =0.754). No significant difference was observed with respect to gender in the development of hypokalemia (p =0.782). Conclusion: This study showed that hypokalemia was a significant clinical manifestation among SARS-COV-2 patients. Further it was noted that treatment regime used for COVID-19 management and gender of the patients are not a risk factor for developing the hypokalemia.

Abstract Background Inflammatory bowel disease involves chronic inflammation and ulceration, primarily Crohn’s disease and ulcerative colitis. The prevalence of inflammatory bowel disease is rising in industrialized countries. We describe the case of a patient with inflammatory bowel disease and multiple electrolyte disturbances that emphasize the link between a vitamin D deficiency and electrolyte imbalances. Case An 86‐year‐old Japanese man with severe hypocalcemia, hypophosphatemia, hypokalemia, and hypomagnesemia was referred to the gastroenterology and hepatology department our university hospital for severe diarrhea and abdominal pain. Based on clinical symptoms and biochemical and endoscopic findings, Crohn’s disease, intestinal Behçet’s disease, and intestinal tuberculosis were considered as differential diagnoses, but a final diagnosis was not reached. Prednisolone, azathioprine, and metronidazole were administered, and no apparent electrolyte abnormality was observed at the patient’s admission to our hospital. On the 80th hospital day, marked hypocalcemia, hypophosphatemia, hypokalemia, and hypomagnesemia were noted and prolonged, despite daily supplementation with Ca and inorganic P. At his consultation with our department, we observed decreased fractional excretion of Ca, tubular reabsorption of phosphate, fractional excretion of K, and fractional excretion of Mg, suggesting the depletion of vitamin D and extrarenal wasting of K and Mg. The patient’s serum Ca and inorganic P were quickly elevated in response to treatment with an active form of vitamin D, and his serum levels of K and Mg were restored to the normal range by an intravenous administration of K and Mg. A vitamin D deficiency is not rare in inflammatory bowel disease and is caused primarily by the decreased intestinal absorption of vitamin D. In the management of electrolyte imbalances in patients with inflammatory bowel disease, clinicians must consider the possible development of vitamin D deficiency-related disorders. Conclusion Vitamin D deficiency in entero-Behçet’s disease leads to severe hypocalcemia and hypophosphatemia, highlighting the importance of awareness in management.

Key Clinical Message Acute neuromuscular paralysis is a relatively common condition in emergency rooms (ERs). They can be caused by several reasons, including adverse drug reactions. Betamethasone is a glucocorticoid commonly used for various conditions, such as allergic conditions. One of the rare but known side effects of glucocorticoids is hypokalemia. Rare cases of hypokalemia following high‐ and low‐dose glucocorticoid injections have been reported. This study presents the history of a young, healthy male without significant past medical history who presented with an inability to stand and walk due to four‐limb paralysis (more prominent in the lower limbs) following an intramuscular injection of a 4 mg betamethasone, which was prescribed for the treatment of allergic rhinitis. The patient was stabilized with an intravascular injection of potassium chloride diluted in 1000 mL of normal saline and monitored for 24 h, ruling out any other endocrine condition. Hypokalemia and its severe form are defined as the serum level of lower than 3.5 and 2.5 mEq/Lit, respectively. One of the etiologies of drug‐induced hypokalemic paralysis is systemic glucocorticoid administration. In severe cases, it can cause quadriplegia and other neuromuscular, respiratory, and cardiac complications. Therefore, it is an urgent condition that should be managed carefully. Pregnant women who are receiving these medications are a specific group at risk of hypokalemic paralysis. There are several safer treatments for seasonal allergic rhinitis compared to systemic glucocorticoids, which should be considered by physicians. Moreover, paralysis in patients receiving these medications should be approached attentively since it might be caused by hypokalemia, which can be life threatening if not treated. It is advisable that the blood level of electrolytes, especially potassium, be checked for patients who present with paralysis or weakness after glucocorticoid injections.

ABSTRACT CONTEXT: Scrub typhus, caused by Orientia tsutsugamushi, has a wide range of clinical manifestations, including meningoencephalitis, acute renal failure, pneumonitis, myocarditis, and septic shock. However, there are no documented cases of scrub typhus with hypokalemia. In this report, we present a case of scrub typhus with hypokalemia and multiple organ failure syndrome, highlighting the importance of electrolyte imbalance in patients with scrub typhus. CASE REPORT: A 59-year-old woman presented to the emergency department with abdominal pain that had been present for 1 day. On admission, the physical examination and laboratory test results indicated that the patient had renal, liver, and circulatory failure, and hypokalemia. She developed meningitis and disseminated intravascular coagulation during hospitalization. She recovered with appropriate management, and was discharged on day 17. CONCLUSION: This report highlights the potential for atypical presentations of scrub typhus, including a previously undocumented association with hypokalemia. Although the contribution of hypokalemia to the patient’s clinical course remains uncertain, this case underscores the importance of considering electrolyte imbalance in the management of patients with scrub typhus. Further research is warranted to better understand the relationship between scrub typhus and electrolyte imbalance.

Bartter Syndrome (BS) is a rare, inherited renal tubulopathy characterised by hypokalaemic, hypochloraemic metabolic alkalosis. Children present with the complaint of polyuria, dehydration, failure to thrive and normal blood pressure despite hyperreninemia and hyperaldosteronism. This is a series of eight children (2 months -1 years of age, 5 males and 3 females children) diagnosed with BS. Mean age of onset was five months with male predominance. Most common presentation was failure to thrive and polyuria. All children showed metabolic alkalosis with hyponatremia, hypokalemia and hypochloremia. Urinary losses of sodium, potassium and chloride were noted in all the eight children. Diagnosis was based on clinical manifestation and electrolyte abnormalities. All children were started on indomethacin and positive response was noted. On follow-up correction of electrolyte abnormalities along with adequate weight gain was seen. Although, it is a rare disease requiring high index of suspicion, but with prompt clinical diagnosis and early treatment, morbidity and mortality can be significantly reduced.

Key Clinical Messages Diagnosis of rare even can be missed due to less familiarity with the disorder. In patients with muscle weakness, infectious causes are prioritized. Electrolyte profile not only identifies the problem, but also prevents unnecessary workup. Abstract In underdeveloped countries, diagnosis of rare disorders is usually delayed due to less familiarity of the clinicians to such disorders. As a result, infectious and inflammatory causes for an ailment are prioritized as compared to non‐infectious etiologies. Hypokalemic periodic paralysis (PP) is a rare disorder, characterized by episodic muscle weakness that can rarely be associated with life‐threatening cardiac arrhythmia. A teenage Afghan boy presented to the emergency department with an acute flaccid paralysis, that started 1 h after intense exercise The weakness involved both, the upper and lower extremities. Laboratory investigations, led to the impression of hypokalemic PP, precipitated by intense exercise. Accordingly, intravenous potassium chloride infusion diluted with normal saline led to the complete resolution of paralysis as well as correction of electrocardiographic changes. The list of differential diagnosis for flaccid muscle paralysis is wide, which generally requires a extensive investigations, but in hypokalemic PP, a cardinal electrolytes profile can lead towards early diagnosis. High degree of clinical suspicion with appropriate history taking and physical examination helps with the immediate identification and management of this disorder.

Ogilvie's syndrome is a rare but potentially life-threatening condition characterised by massive dilation of the colon without a mechanical obstruction. It typically affects older adults and those with underlying medical conditions, such as neurological or cardiovascular diseases, and may result in severe complications such as perforation or sepsis. Diagnosis is based on clinical presentation and radiological studies, and treatment involves a combination of conservative measures, such as bowel rest and pharmacological agents, and interventional procedures, such as endoscopic decompression or surgery. Here we present the case of a 67 year old male who presented with Ogilvie’s syndrome after changes in his antipsychotic medications. He was given laxatives which led to persistent hypokalemia contributing to worsening distention. This case report highlights the important aspects in management such as cautious use of secretory laxatives (causing worsening Hypokalemia) and combination of motility agents in pseudo colonic obstruction.

Renal tubular acidosis is an tubule-interstitial disease, which is a rare cause of hypokalemia in clinical practice. At present, primary mesangial proliferative glomerulonephritis complicated with renal tubular acidosis have been rarely reported. In this article, one 34-year old male patient with recurrent polyuria and limb weakness for 10 years, followed by 1 day as chief complaint, was reported. He developed nocturia and hypokalemia 10 years ago, with negative urinary protein and normal blood albumin and estimation of glomerular filtration rate （eGFR）. Five years ago, he developed lower limb edema and positive urinary protein. Kidney biopsy showed primary mesangial proliferative glomerulonephritis. The symptoms of lower limb edema and hypokalemia recurred 1 day. Urinary acidification function test indicated renal tubular acidosis. Potassium supplement, diuresis and hormone therapy were given to effectively relieve the condition. The diagnosis and treatment of this case suggest that primary mesangial proliferative glomerulonephritis can be complicated with renal tubular acidosis. Attention should be paid to avoiding missed diagnosis. Interventions for renal tubular acidosis combined with timely hormone therapy yield high clinical efficacy.

Key Clinical Message An underlying autoimmune condition should be suspected in patients who presented with periodic muscular weakness secondary to distal RTA that leads to hypokalemia because distal RTA is commonly associated with autoimmune disorders such as Sjögren's syndrome. Abstract A 22‐year‐old female presented with a sudden onset of bilateral weakness in both upper and lower limbs. The patient had a history of muscular weakness secondary to hypokalemia and dryness of the eyes for the last 3 years. Laboratory investigations revealed decreased potassium and metabolic acidosis. Further investigations confirmed distal renal tubular acidosis (RTA) and Sjögren's syndrome. A diagnosis of distal RTA secondary to Sjögren's syndrome was made. Her potassium levels were replaced, and she was discharged with oral potassium supplements, steroids, and artificial tears.

Hypokalemia is a common electrolyte disorder in cancer patients that may be associated with the primary disease or a complication of treatment. In this article, we provide a brief description of hypokalemia and its appropriate management in cancer patients.

Hypokalemia is a common electrolyte abnormality often encountered in daily practice. While mild hypokalemia often asymptomatic, moderate-to-severe hypokalemia usually manifested as significant symptoms such as muscle weakness. In this paper, we presented a case of 23-years-old male coming to our emergency department because of muscle weakness in all his four limbs when he woke up in the morning. Physical examinations were all within normal limit, except that his muscle strength decreased in all four extremities. Laboratory measures showed severe hypokalemia (1.9 mmol/L), hence patient was treated with potassium infusions. During hospitalization, thyroid function tests revealed hyperthyroidism. Therefore, in patient with paralysis, in which laboratory finding showed hypokalemia, hyperthyroidism should be considered as one of the potential diagnosis especially in younger patient, even in patient without previous history of hyperthyroidism. Merely treating hypokalemia in patient with underlying hyperthyroidism could be a dangerous boomerang.

Background The Portland intensive insulin therapy effectively controls acute hyperglycemic change after graft reperfusion during liver transplantation. However, the time-consuming sophistication acts as a barrier leading to misinterpretation and decreasing compliance to the protocol; thus, we newly introduced an application software “Insulin protocol calculator” which automatically calculates therapeutic bolus/continuous insulin doses based on the Portland protocol. Methods Of 144 patients who underwent liver transplantation, 74 patients were treated before the introduction of "Insulin protocol calculator" by using a paper manual, and 70 patients were treated by using the application. Compliance was defined as the proportion of patients treated with exact bolus/continuous insulin dose according to the Portland protocol. Results Compliance was significantly greater in app group than in paper group regarding bolus dose (94.5% and 86.9%, P < 0.001), continuous dose (88.9% and 77.3%, P = 0.001), and both doses (86.6% and 73.8%, P < 0.001). Blood glucose concentration was significantly lower in app group at 3 h (125 ± 17 mg/dl vs. 136 ± 19 mg/dl, P = 0.014) and 4 h (135 ± 22 mg/dl vs. 115 ± 15 mg/dl, P = 0.029) after graft reperfusion. Acute hyperglycemic change during 30 min was more prominent in app group while hyperglycemia incidence was 71.4% vs. 54.1% (P = 0.031). However, hyperglycemia risk was comparable at 2 h (31.4% vs. 31.1%, P = 0.964), and even insignificantly lower in app group at 3 h (7.1% vs. 19.5%, P = 0.184). Conclusions Compliance to the Portland protocol was significantly improved after introducing the application software; post-reperfusion hyperglycemia was better controlled. “Insulin protocol calculator” is cost-effective and time-saving with potential clinical benefits.

This article reported a 38-year-old female patient who was misdiagnosed as Sjögren’s syndrome complicated with type I distal renal tubular acidosis （dRTA） due to recurrent hypokalemia, alkaline urine, elevated urinary potassium, positive antinuclear body（ANA）, and positive anti-SSA antibody. The diagnosis of Sjögren’s syndrome was then excluded because the patient had no obvious dry mouth or dry eyes, and the results of unstimulating saliva flow rate, corneal fluorescence staining, Schirmer secretion test, or labial gland biopsy were all negative. The clinical manifestations, such as metabolic alkalosis, hypochloremia, hypomagnesemia and low urinary calcium,could not support the diagnosis of dRTA. The patient presented with severe hypomagnesemia and a Trousseau sign, then Gitelman syndrome was finally confirmed based on genetic testing. Therefore, the diagnosis and treatment of this case prompted that for patients with recurrent hypokalemia and positive anti-SSA antibody, clinicians should make differential diagnosis based on the acid-base imbalance and the electrolyte disturbance at first, instead of paying too much attention to autoantibodies and Sjögren’s syndrome, to avoid being misled by the ANA and anti-SSA antibody.

Adult-onset Still’s disease (AOSD) is a rare autoinflammatory disorder that can lead to a cytokine storm, causing a range of symptoms. Acute intestinal pseudo-obstruction is another rare condition that results in intestinal obstruction without anatomical cause. Although the two conditions are rarely reported together, we present the case of a 62-year-old male who developed acute intestinal pseudo-obstruction in the context of an AOSD flare. This led to severe hypokalaemia and a critical condition. Other symptoms included a high-spiking fever lasting for weeks, polyarthralgias and a typical salmon-coloured rash. After ruling out other potential causes, the patient was diagnosed with AOSD. Our findings suggest that the cytokine storm associated with this disease triggered the acute intestinal pseudo-obstruction and life-threatening hypokalaemia, establishing a causal relationship. Only four other cases of AOSD complicated by intestinal pseudo-obstruction have been reported, and this is the first to present with life-threatening hypokalaemia. This case serves as a crucial reminder that, despite being a diagnosis of exclusion, Still’s disease should be considered as a potential cause of intestinal pseudo-obstruction, as prompt recognition and treatment of the underlying cause is crucial in managing this potentially life-threatening condition.

Intractable hypokalemia and hypocalcemia are rare complications in leukemia patients. This article reports a patient with chronic myelomonocytic leukemia (CMML)with refractory hypokalemia, hypocalcemia, hypochloridemia, hypomagnesemia-a 48-year-old man complained of fatigue, nausea, and face numbness for over one month. The number of monocytosis in peripheral blood and bone marrow increased remarkably. At the same time, the patient developed hypokalemia, hypochloridemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, massive proteinuria, and increase in plasma aldosterone and renin. After two coursea of treatment using Azacitidine therapy, complete remission of bone marrow was achieved and the electrolyte disturbance was almost corrected, except hypomagnesemia. We summarize the clinical characteristics of the patient so as to raise the clinical awareness of such cases.

Thyrotoxic periodic paralysis (TPP) is an endocrine emergency caused by thyrotoxicosis, mainly manifesting as periodic muscle weakness and hypokalemia, which seriously threatens the health of patients. The level of hypokalemia is closely related to the severity of muscle weakness in patients with TPP, and potassium supplementation can quickly alleviate the symptom of muscle weakness and hypokalemia. However, excessive potassium supplementation can lead to acute rebound hyperkalemia in patients with TPP, which also threatens the health of patients. This article reported 3 cases of TPP patients with acute rebound hyperkalemia caused by excessive potassium supplementation, and analyzed the risk factors for rebound hyperkalemia, in order to provide more information for the clinical treatment of TPP patients.

Abstract Background Capecitabine is widely used in chemotherapy for breast, colorectal, and gastric cancers. The frequent adverse reactions of capecitabine mainly include gastrointestinal side effects, anemia, and cardiovascular toxicity. Here, we report a rare case of severe hyperglycemia and hypokalemia during long-term treatment with capecitabine. Case presentation A 48-year-old Chinese female was hospitalized with the complaint of breathlessness and weakness after activity, for 1 month. Her past history is significant for a diagnosis of right-sided breast cancer 7 years ago. She underwent right mastectomy, following which capecitabine was started 1.5 years prior to the current admission as part of her primary treatment at the discovery of systemic osseous metastasis. Her fasting plasma glucose and hemoglobin A1c levels were quite normal 7 months ago but increased to 15.3 mmol/L and 11.2%, respectively, at the present admission. Her serum potassium level was as low as 2.5 mmol/L. Plasma autoantibodies related to islets and insulin were all negative. Capecitabine was discontinued, and an insulin pump and potassium supplement were given after admission. Her blood sugar and potassium levels returned to their normal ranges soon. Self-injection of insulin was withdrawn completely at 2 months after discharge, and no oral hypoglycemic agents were added. Her plasma glucose and electrolyte levels were at normal levels at her 1-year follow-up. Conclusion Glucose intolerance and hypokalemia may be rare but serious adverse effects during long-term chemotherapy with capecitabine.

Background: The association between thyroid dysfunction and electrolyte imbalance may result in significant morbidity. The present study was conducted to evaluate the effect of hypothyroidism on serum potassium levels in an urban female population of Eastern India. Materials and Methods: The present study was conducted in a peripheral Medical College in West Bengal for 12 months after taking Institutional Ethical Clearance and informed consent of the participants. One hundred and fifty hypothyroid females were included in the study group and one hundred participants were included as a control. The participants of both groups were age-matched. Serum thyroid-stimulating hormone (TSH) and free thyroxine 4 (FT4) levels were estimated by the enzyme-linked immunosorbent assay method and serum potassium was estimated by ion-selective electrode. Unpaired t-test and correlation coefficient were used for the analysis of data. Results: Hypokalemia was observed in 23 participants among the 150 hypothyroid females included in the study (15.33%). There was a significant difference in TSH (P < 0.00001), FT4 (P < 0.00001), and potassium levels (P = 0.000031) between the study and control groups. Serum potassium levels were strongly negatively correlated with TSH levels (r = −0.7356, P < 0.00001), the R2 value of 54.11%, and positively correlated with FT4 levels (r = 0.224, P = 0.005859). Conclusions: 15.33% of hypothyroid females included in the study had hypokalemia and serum potassium levels were significantly less in hypothyroid females as compared to euthyroid controls and serum potassium levels were negatively correlated with TSH levels. Serum electrolyte estimation may be of considerable importance in the management of hypothyroid individuals and needs to be considered and may help to prevent further possible complications.

Introduction: Pathophysiological changes secondary to cirrhosis predispose patients of chronic liver disease to develop various electrolyte disturbances which have a significant impact on morbidity, mortality, and prognosis of these patients. This study aims to estimate the level of electrolyte disturbance and its association with the severity, complication, and outcome in chronic liver disease patients attending a hospital in the Kumaon region of Uttarakhand. Methods: Our study was a hospital-based cross-sectional study conducted on 100 chronic liver disease patients at the OPD/IPD Department of Medicine, Dr. Sushila Tiwari Hospital, Haldwani, Uttarakhand, from January 2020 to September 2021. Results: Hyponatremia was observed in 49% of the patients, hypokalemia in 30%, and hypocalcemia in 16% of the patients. The electrolyte levels were similar irrespective of the disease severity and presence of complications. The sodium and potassium levels had a significant association with the outcomes. Conclusion: Hyponatremia was the commonest electrolyte disturbance seen in the study patients. No significant association was observed between the electrolyte and severity of the disease and complications.

Abstract Background Acquired long QT syndrome is an important and preventable cause of cardiac arrest. Certain medications and electrolyte disturbance are common contributors, and often coexist. In this case, we report five contributors to cardiac arrest. Case presentation This case is of a 51-year-old Caucasian female patient who presented with vomiting associated with hypokalemia and hypomagnesemia. She subsequently received ondansetron and metoclopramide, on the background of chronic treatment with fluoxetine. She then suffered an in-hospital monitored cardiac arrest, with features of long QT and torsades de pointes retrospectively noted on her prearrest electrocardiogram. She was diagnosed with acquired long QT syndrome, and her QT interval later normalized after removal of offending causes. Conclusions This case highlights the importance of proper consideration prior to prescribing QT prolonging medications, especially in patients who have other risk factors for prolonged QT, such as electrolyte disturbances and pretreatment with QT prolonging medications.

The periodic paralyses (PPs) are a group of rare neuromuscular disorders related to muscle ion channels, presenting with episodes of sudden muscle weakness. The majority of cases of PP are inherited, resulting from genetic mutations in the subunits of channel proteins of the sodium, potassium, or calcium channels or the SCL4A1 protein. We describe two siblings, a 15-year-old male and an 11-year-old male, presenting with complaints of weakness. Both patients had consumed a large carbohydrate-rich meal the previous night with a history of similar episodes of weakness suggesting a diagnosis of PP. Laboratory investigations were unremarkable except for hypokalemia in both patients, and they were started on potassium supplementation, which resulted in the resolution of symptoms. The elder sibling was started on acetazolamide for prophylaxis, but due to non-response, was put on spironolactone which he tolerated well. Genetic mutation analysis confirmed the diagnosis of familial hypokalemic periodic paralysis (FHPP) with a p.Arg672His mutation in the sodium channel, gene SCN4A (17q23.3) in both siblings. The diagnosis of PP is important to consider in patients with sudden recurring episodes of weakness or paralysis, especially in otherwise healthy adolescents/young adults. The treatment of FHPP is challenging, with cautious potassium supplementation for acute attacks. Workup for other causes should be performed, and genetic analysis is recommended to confirm the diagnosis.

Abstract Herein we report the intriguing case of a 42‐year‐old woman presenting with grade three hypertension, severe hypokalemia and primary amenorrhea, which revealed to be the complete form of 17 alphahydroxylase deficiency. We also discuss the challenging therapeutic approach as well as the outcomes and the follow‐up of this patient.

Background. Gitelman syndrome (GS) is an inherited salt-losing renal tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. Patients can be asymptomatic until late adolescence or adulthood, and hence may be discovered incidentally during presentation with other illnesses. GS has been described in association with thyroid disorders and should be considered in patients with hyperthyroidism and persistent hypokalemia, especially in those with associated hypomagnesemia and hypocalciuria. Case summary. In this report, we describe an 18-year-old female who presented with hyperemesis gravidarum and thyrotoxicosis, and was incidentally found to have GS, confirmed by the sequence analysis of SLC12A3. Conclusions. Thyroid dysfunctions, such as hypothyroidism, thyrotoxicosis, and thyroid nodules, may develop during pregnancy. A structural homology between the beta-human chorionic gonadotropin and thyroid stimulating hormone molecules, as well as their receptors is probably the basis for the transient thyrotoxicosis crisis during pregnancy. Since hyperemesis in pregnancy can also lead to hypokalemia and alkalosis, a high index of suspicion for GS during pregnancy is required for timely diagnosis and management.

Background: Patients with cirrhosis may have either a chronic neuropsychiatric state due to portal-systematic shunting or have an acute episode with some precipitating factor labeled as hepatic encephalopathy. In patients with encephalopathy, hypokalemic alkalosis leads to an increase in the amount of nonionic ammonia that readily crosses the blood brain barrier and accumulates in the CNS that can worsen the disease. Objective: The purpose of the study was to determine the frequency of hypokalemia in patients with hepatic encephalopathy and to compare the length of the hospital stay in hepatic encephalopathy patients with and without hypokalemia. Study type, settings & duration: This cross sectional study was conducted at Jinnah Postgraduate Medical Centre, Karachi from February to July 2021. Methodology: The sample was calculated by using WHO sample size calculator at 95% confidence interval and absolute precision of 8% with anticipated population proportion of 35%. The sample was recruited by using non-probability consecutive sampling technique. Hepatic encephalopathy was diagnosed on basis of clinical examination by West Haven Classification grades. Patients were diagnosed for hypokalemia by hospital lab as having potassium levels

A 28-year-old female patient was hospitalized for mild–moderate hypokalaemia which was persistent despite discontinuation of beta-2 agonist bronchodilator treatment. Her past medical history was relevant for two episodes of severe hypokalaemia after active inhaled beta-2 agonist treatment for asthma crisis. Investigations revealed increased potassium in spot urine with a transtubular potassium gradient

Abstract Background Acetamiprid is a potent new first-generation neonicotinoid insecticide in agricultural practices. It is well described that it has low toxicity among animals and is lethal if consumed in large amounts. However, toxicity in humans is rarely reported in literature. Here, we describe acetamiprid toxicity complicated with severe lactic acidosis, myocardial ischemia, refractory hypotension, and severe hypokalemia in a middle-aged man who presented with deliberate self-harming with acetamiprid poisoning in Sri Lanka. Case presentation We describe a case of acute poisoning with an acetamiprid in a middle-aged Sri Lankan Tamil farmer for suicidal purposes following family conflicts with his wife. He presented with severe nausea, vomiting, and altered level of consciousness. He had electrocardiogram changes, hypoxia, and lactic acidosis. With intensive care management including ventilatory support, inotropic therapy along with intraarterial blood pressure monitoring, correction of acidosis, and administration of electrolytes, he made good clinical recovery. He was discharged without any further complications 6 days after ingestion of acetamiprid. Conclusions This case illustrates a rare, acute poisoning with acetamiprid in human, as well as its clinical manifestations and successful management with supportive therapy. This will be helpful for clinicians to identify clinical manifestations and to guide management of acute poisoning with acetamiprid in the future.

Various conditions causing weakness associated with coronavirus disease 2019 (COVID-19) infection have been described, including cerebrovascular diseases, acute myelitis, Guillain-Barré syndrome, myasthenia gravis, critical illness myopathy and neuropathy, myositis, and rhabdomyolysis. We report an adult man presenting with an unusual etiology of weakness after a COVID-19 infection. Thyrotoxic hypokalemic periodic paralysis (THPP) was diagnosed from the presence of Graves' disease and hypokalemia because of intra-cellular potassium shifting. His weakness and hypokalemia responded well to potassium supplements and a non-selective b-blocker, whereas his thyrotoxicosis was initially controlled by an anti-thyroid medication and subsequently with radioactive iodine therapy. He was also treated as having mild COVID-19 based on his normal chest X-ray and oxygenation level. This is the first report showing an association between COVID-19 infection and a paralysis attack of THPP. Physicians should be alerted about this unusual cause of weakness, particularly in Asian patients.

Abstract We report a young adult woman with 17 alpha‐hydroxylase deficiency (17α‐OHD) in Shandong province of China. The patient carried compound heterozygous mutations in the CYP17A1 gene: c.985–987 delinsAA (p.Tyr329LysfsX90) and c.1486C > T (p.Arg496Cys). The patient's hypertension and hypokalemia were resolved after taking medications of glucocorticoid, aldactone, and calcium antagonists.

Abstract Background Hypokalemia has been rarely attributed to tizanidine, although the precise mechanism is unclear. Severe hypokalemia is a well-established cause of abnormalities involving cardiac conduction. Given this agent’s well-known cardiac arrhythmogenic potential, awareness of potential concomitant electrolyte abnormalities is important. Case presentation Electrolyte disorders, including hypokalemia, are rare complications of the antispasmodic medicine tizanidine when taken in doses as outlined by the manufacturer’s prescribing instructions. Although cases of severe hypokalemia have also been described in the literature in association with this agent, such reports are few. We report a Caucasian case of an intentional overdose involving a very large ingestion of tizanidine. In addition to the characteristic abnormalities on the electrocardiogram, our patient developed electrolyte derangements as well as self-limited acute kidney injury. These biochemical abnormalities included profound hypokalemia that was refractory to aggressive replacement over the ensuing several days, before eventually dissipating. A thorough assessment of the etiology of this hypokalemia was consistent with a defect in renal potassium handling. Conclusion In our patient with intentional tizanidine overdose, severe and refractory hypokalemia appears to have been due to a transient potassium wasting nephropathy.

Hypomagnesemia is an electrolyte disorder associated with decreased nutritional intake, gastrointestinal losses, and renal clearance of magnesium, a divalent cation that, having a higher concentration at the intracellular level, makes it difficult to analyze its absolute deficit and establish an adequate correction that supplies daily losses and requirements; For this reason, knowledge of the etiologies of hypomagnesemia, as well as the calculation of the excreted fraction of magnesium and measurement of magnesiuria in 24 hours, are useful tools to establish adequate guidelines for continuous magnesium correction, in order to avoid complications associated with its toxicity or poor correction that perpetuates this electrolyte disorder, and generates the appearance of symptoms as severe as tetany and ventilatory failure. These severe manifestations were resent in the patient described, who, in the absence of shock or base acid disorder, required admission to the intensive care unit for invasive mechanical ventilation and correction of their electrolyte disorders associated with ulcerative colitis (hypocalcemia, hypokalemia, and hypomagnesemia).

Key Clinical Message Abnormal acid‐base status (metabolic acidosis or alkalosis), inappropriate urine electrolytes excretion (high or low Na+ and Cl−), and higher required dose of potassium supplement (4‐5 mmol/kg) are suggestive of non‐TPP causes of hypokalemia.

Abstract Background Primary adrenal insufficiency (Addison's disease) is a rare medical condition usually associated with hyperkalemia or normokalemia. We report a rare case of Addison's disease, coexisting with hypokalemia, requiring treatment. Case presentation In this case, a 42-year-old man was admitted to the intensive care unit with a history of loss of consciousness and severe hypoglycemia. His blood tests showed metabolic acidosis, low concentrations of cortisol 6 nmol/L (normal 68–327 nmol/L), and high plasma adrenocorticotropic hormone 253 pmol/L (normal 1.6–13.9 pmol/L), and he was diagnosed with primary adrenal insufficiency. Surprisingly, his serum potassium was low, 2.3 mmol/L (normal 3.5–5.1 mmol/L), requiring replacement over the course of his admission. Computed tomography scan of the adrenal glands showed features suggestive of unilateral adrenal tuberculosis. Investigations confirmed renal tubulopathy. The patient responded favorably to cortisol replacement, but never required fludrocortisone. Conclusions Coexistence of hypokalemia with Addison’s disease is unusual. We recommend investigation of the cause of hypokalemia in its own right, if it occurs with primary adrenal insufficiency.

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism, often presents with limb muscle paralysis, hypokalemia with elevated-free T3, T4, and low thyroid-stimulating hormone (TSH). We herein reported an unusual presentation of TPP with acute hypercapnic respiratory failure. A 28-year-old female had complaints of nausea and vomiting. Laboratory investigations showed a serum potassium level of 1.2 mEq/L. Thyroid function test revealed the TSH level of 0.021 μlU/mL and free T4 at 2.01 ng/dL. She suddenly suffered from dyspnea and drowsiness. Acute hypercapnic respiratory failure with CO2retention was found. Noninvasive ventilation was used. Rapid correction of hypokalemia and administration of propylthiouracil, propranolol, and 5% Lugol's solution were performed. After the normalization of potassium levels, the patient's respiratory pattern stabilized and noninvasive ventilator (NIV) use was discontinued. Respiratory failure is an unusual but lethal complication of TPP. Rapid correction of hypokalemia and temporarily NIV can successfully avoid endotracheal intubation for respiratory failure.

Abstract Thyrotoxic periodic paralysis (TPP) is rarely seen in children and adolescents. Clinical manifestations in children and adolescents may vary. It is important for clinicians to be aware of this rare and life‐threatening condition.

Abstract Maternal diet before and during pregnancy plays an important role for the developing fetus. Any eating disorder in this period can cause transient or/and permanent negative effects on the mother and her offspring.

Abstract Posaconazole therapy may lead to increased serum estradiol levels and development of gynecomastia. Early detection by endocrine hormone measurements may help preventing gynecomastia.

Objective: To find out the frequency of intensive care unit acquired hypernatremia in critically ill patients and to find out the outcomes in terms of mortality/discharge with respect to age and gender. Study Design: Cross sectional study. Place and Duration of Study: Medical, trauma and surgical intensive care unit settings of Combined Military Hospital Kohat, from Jun 2018 to Jun 2019. Methodology: A total of 100 patients were enrolled who were normonatremic at the time of intensive care unit admission. Patients were followed for 2 weeks of their stay for intensive care unit acquired complications and mortality. Serum sodium levels along with other investigations were carried out on daily basis from a single pathology laboratory. Data including the clinical diagnosis, APACHE II score and intensive care unit acquired complications was recorded on a proforma. Data was analyzed using SPSS version 22 and Microsoft Excel 365. Results: The frequency of intensive care unit acquired hypernatremia was 46 (46%) further classified into mild 13 (13%), moderate 15 (15%) and severe 18 (18%) hypernatremia. The overall mortality was 30 (30%), 10 (18.5%) and 20 (43.5%) cases in normal and raised serum sodium group respectively. We reported a slightly higher frequency of Intensive care unit acquired hypernatremia in our study. The mortality was also significant in hyponatremic group. Conclusion: Intensive care unit acquired hypernatremia was an invaluable marker for quality health care in critically ill patients and it’s also an important risk factor for Intensive care unit associated mortality.

Obesity is a common health problem and the prevalence is increasing worldwide. The improper and unregulated use of unconventional therapies, especially herbal treatment methods, has grown due to widespread availability. In our case, a 41-year-old male patient developed palpitation, confusion, loss of consciousness, and cardiac arrest while at home. An emergency medical team was called and chest compressions were performed by his wife until the medical team arrived. Ventricular fibrillation was detected on the monitor 5 minutes after the cardiac arrest occurred and the patient was defibrillated. A physical evaluation revealed hypotension and tachycardia. Electrocardiography (ECG) showed a fast idioventricular rhythm with capture and fusion beats and evident J waves in leads DII, DIII, and aVF. Brain magnetic resonance imaging and thoracic tomography revealed no pathology to explain his clinical condition and the coronary angiography results were not significant. The laboratory parameters included potassium (K): 2.23 mEq/L, ionized K (arterial blood): 2.43 mEq/L, sodium: 142 mEq/L, calcium: 9.3 mg/dL, creatinine: 1.6 mg/dL, pH: 7.29, cardiac troponin I: 0.12 (normal range: 0–0.11 ng/mL) and creatinine kinase mass: 8.3 (normal range: 0–3.23 ng/mL). After fluids and electrolyte replacement therapy were administered, the ECG results revealed narrow QRS complex atrial fibrillation followed by a normal sinus rhythm with a 490 ms corrected QT interval. The patient was extubated in follow-up. There were no risk factors for coronary artery disease, no history of drug or other substance use, and no exposure to excessive emotional or physical stress. The patient said that he had been consuming a large quantity of teff tea for 5 days to lose weight. He was discharged without any complications and has been asymptomatic in 9 months of follow-up. The inappropriate use of weight loss alternatives, especially herbal therapies such as teff tea, and the incidence of associated side effects are increasing due to wide availability and easy access. The general population should be warned about this issue.

Objective To investigate the mechanism of arrhythmia induced by pantoprazole (PPZ) in mice with hypokalemia. Methods Mice were randomly divided into control group, PPZ group [20 mg/(kg·d), intraperitoneal injection for 5 weeks], furosemide (FS) group and FS+PPZ group. After 5 weeks, the ECG parameters (heart rate, PR interval, QRS interval, QTc interval) and spontaneous arrhythmia were monitored. The changes of the mRNA and protein expression of hyperpolarization-activated and cyclic nucleotide-cation channels 2 and 4 (HCN2 and HCN4), cardiac voltage-gated sodium channel alpha subunit (SCN5A), L-type calcium channel alpha subunit (CACNA1C) and T-type calcium channel alpha subunit (CACNA1G) were analysed by real-time fluorescence quantitative PCR and Western blot technology. Results Compared with control group, the HR was significantly decreased and PR interval was prolonged in PPZ group (P＜0.01, P＜0.05). Compared with FS group,the HR and PR interval in FS+PPZ group were further decreased and prolonged (P＜0.01, P＜0.05), and 4 mice developed sinus arrest (SA) (P＜0.05). The expressions of HCN4 mRNA and protein in PPZ group were lower than those in control group (P＜0.01), respectively, and the expression in FS+PPZ group was lower than those in FS group (P＜0.01). The expression of HCN2 mRNA in PPZ group was lower than that in control group(P＜0.05), which was further decreased in FS+PPZ group compared with FS group (P＜0.01). Conclusions It is found that pantoprazole may lead to bradyarrhythmia in mice under hypokalemia, which may be related to abnormal expression of HCN2 and HCN4.

Abstract Background In clinical practice, both the history and laboratory testing are paramount to making an accurate diagnosis. Situations in which laboratory findings and patient history are not congruent pose a diagnostic dilemma. We report a case of a young woman presenting with a myriad of electrolyte and acid-base disorders. Difficulty in reaching a unifying diagnosis persisted due to discordant patient history. We believe this case shows that lab findings will clearly portray the problems a patient has and should be given more credence in a case where the history is discordant with lab findings. Case presentation A 28-year-old Hispanic American woman presented to the emergency room of our institution with a complaint of painless and sudden onset of stiffness in her upper and lower limbs. Associated weakness worse in the distal limbs was also reported. She experienced shortness of breath with minimal exertion, diaphoresis, and anxiety. Her vital signs revealed tachycardia without corresponding fever. She was conscious, oriented, and alert. Her physical exam revealed dry mucous membranes and warm extremities. She denied recent consumption of a large carbohydrate meal, diarrhea, vomiting, use of laxatives, and use of alcohol or recreational drugs. She vaguely described two previous similar episodes in the last 7 months that spontaneously resolved. Her medical history was significant only for hypothyroidism treated with daily levothyroxine tablets. Laboratory analysis revealed the following abnormalities: an elevated anion gap with significant lactate, hypokalemia, hypomagnesemia, elevated mean corpuscular volume, elevated mean cell hemoglobin, and elevated liver enzymes with aspartate aminotransferase/alanine aminotransferase ratio > 2. She was hydrated with balanced crystalloids, and her electrolyte deficiencies corrected. The etiology of her multiple electrolyte abnormalities was unclear because alcohol use was vehemently denied. Extensive evaluation for causes of electrolyte disorder was undertaken, which was unrevealing. On further interrogation, she admitted to recent alcohol intoxication and several episodes of vomiting before presentation. She was advised to refrain from alcohol use and discharged afterward. Conclusion Both patient history and laboratory analysis have a role in identifying and confirming a diagnosis. In cases in which laboratory tests are incongruous with reported history, making a unifying diagnosis can be challenging or delayed. The importance of taking a comprehensive history cannot be overemphasized, but history provided by patients may be prone to intentional or unintentional distortion, whereas laboratory findings are more objective. The case presented underscores why the lab findings should be given credence in cases in which there is discordance between lab results and the provided patient history.

Primary hyperaldosteronism (PA) is the most common cause of secondary arterial hypertension and is frequently undiagnosed. It affects all ages but is more frequent between 20 and 60 years old. The clinical presentation is variable, and the diagnosis is based on screening and, in equivocal cases, confirmatory tests. A 19-year-old student presented with complaints of extreme fatigue, arterial hypertension, hypokalemia and metabolic alkalosis, raising a high index of suspicion for PA. Screening tests were performed and its expressiveness excluded the need of confirmatory tests. CT-scan showed a unilateral adrenal adenoma and the patient was submitted to laparoscopic adenectomy without complications. Prompt diagnosis and treatment are essential to avoid long term complications of PA.

Abstract Primary aldosteronism (PA) is a potentially reversible cause of uncontrolled hypertension. Early diagnosis and timely management of PA can prevent end‐organ damage. Aldosteronoma Resolution Score (ARS) is a useful tool to predict cure rates and resolution of hypertension after adrenalectomy.