A word of caution regarding Ceftriaxone

Ceftriaxone is a well-known antibiotic belonging to the third generation of cephalosporins. This broad-spectrum drug is highly effective against gram negative and gram-positive bacterial infections and is frequently used to treat severe bacterial infections in pediatrics, including disseminated gonococcal infections, sepsis and meningitis. However, concerns have been raised regarding the drug’s safety as it is prone to various side effects like bilirubin encephalopathy, cholestasis, pseudolithiasis and rarely hepatitis and pancreatitis.1 A prospective study in 154 children published in Human and Experimental Toxicology in 2016 further validate this point.2 According to this study, out of 84, 20.9% children treated with ceftriaxone had abnormal biliary sonographic findings and 15.1% had biliary lithiasis whereas cefotaxime was found to be comparatively safer. Worrying facts related to Ceftriaxone should definitely be taken into consideration as ceftriaxone is a standard treatment for several bacterial infections in children and is being prescribed at a regular basis in many countries. In fact, a clinical study performed in a secondary care hospital of Karachi, Pakistan, declared it the most frequently prescribed antibiotic.3 Physicians should prescribe ceftriaxone with caution. Ceftriaxone should be avoided in neonates especially those with hyperbilirubinemia. Caution must be advised for the use of intravenous ceftriaxone with intravenous calcium containing solutions as their concomitant use can lead to life threatening adverse reactions.4 Patient should seek medical help if they experience diarrhea, jaundice, confusion, headache, heart palpitations etc. Similar drugs with a safer adverse effect profile should be considered as a future alternative. Continuous..

Concomitant Ceftriaxone and Intravenous Calcium Therapy in Infants

OBJECTIVE To determine if increased mortality could be detected with the administration of ceftriaxone and IV calcium in infants through an analysis of a large repository of electronic health records. METHODS Patients were split into 3 groups: 1) neonates, 2) infants, and 3) infants <1 year whose age was not specified. Deaths were classified into mutually exclusive categories based on the administration and timing of ceftriaxone and IV calcium. Crude death rates were calculated, and logistic regression modeling was used to calculate adjusted relative odds of death with associated covariates. RESULTS A total of 259,149 infants were identified. Of 79,038 neonates, the proportion of patients that received ceftriaxone and IV calcium within 48 hours who died was 3.8%, compared with 1.95% (IV calcium), 0.3% (ceftriaxone), 1.54% (IV fluids), and 2.03% (parenteral nutrition). For 102,456 infants, the proportions of deaths were 5.47% (ceftriaxone and IV calcium within 48 hours), 0.45% (IV calcium), 0.15% (ceftriaxone), 0.39% (IV fluids), and 5.5% (parenteral nutrition). Multivariate analysis showed increased odds of death in infants who received ceftriaxone and IV calcium within 48 hours, regardless of age, and propensity score–matched analysis showed a more than 2-fold increased risk for death. CONCLUSIONS The increased risk for death following ceftriaxone and IV calcium administration was noted not only in neonates, but among older infants as well.

Lead encephalopathy in an adult opioid abuser

A 38-year-old man presented at the emergency department with abdominal pain, vomiting, generalised weakness and altered consciousness. He had been ingesting opioids for over 5 years and had several past hospital admissions for abdominal pain. His investigations showed deranged liver function tests, anaemia and basophilic stippling on the peripheral blood smear. Further investigations revealed a significant increase in the serum lead level. We started chelation with peroral penicillamine 250 mg every 6 hours for 2 days and switched to intramuscular dimercaprol 4 mg/kg every 12 hours and intravenous calcium ethylenediamine tetraacetic acid 50 mg/kg in two divided doses daily for the next 5 days. We then discharged him home; he had become clinically stable by that time. We repeated his lead level and followed him up in the clinic. In this report, we emphasise the consideration of lead toxicity in opioid abusers and bring to attention a rare way of lead chelation in resource-limited settings.

Hypocalcemia as a Cause of Complex Febrile Seizures in a Toddler

A 13-month-old boy had suffered three episodes of complex febrile seizures. At this admission, there were signs of hyperexcitability, such as Trousseau sign and QTc prolongation. A point of care blood gas analysis revealed severe hypocalcemia. Therefore, prior to administering intravenous calcium gluconate, we took blood samples to investigate the etiology of this hypocalcemia: magnesium, parathormone, and 25-hydroxyvitamin D. Since both parathormone and phosphate were significantly elevated and 25-hydroxyvitamin D was within the normal range, pseudohypoparathyroidism was diagnosed. After two years of follow-up, serum calcium had normalized in our patient under supplementation of vitamin D and calcium. He had been free of convulsions, although different febrile episodes had occurred.

Hypocalcemia in a 15 Year Old With New Onset Type 2 Diabetes Mellitus

Background: Diabetic ketoacidosis and significant hyperglycemia are associated with known electrolyte derangements in sodium, potassium, and phosphorus. Hypocalcemia and hypoparathyroidism occurring in uncontrolled diabetes are rare. We present a case of new-onset diabetes with severe hypocalcemia. Case: A 15-year-old obese Caucasian male with ADHD and autism presented to the Emergency room due to hyperglycemia found on laboratory evaluation for hypertension. Serum glucose was 563 mg/dL, serum bicarbonate 24 meq/L (21 - 31 meq/L), and HgbA1C 11.4% (4.0 - 5.6%). He was admitted to initiate insulin and for diabetes education. On admission, hypocalcemia was noted: serum calcium 6.6 mg/dL (8.5 - 10.5 mg/dL), alkaline phosphatase 352 units/L (48 - 277 units/L), and albumin 4.6 g/dL (3.5 - 5.0 g/dL). Repeat testing revealed serum calcium 5.1 mg/dL, phosphorus 4.3 mg/dL (2.5 - 4.5 mg/dL), and magnesium 1.7 mg/dL (1.6 - 2.9 mg/dL). He endorsed a 2 month history of tetany, paresthesia, and muscle weakness. Due to food aversions, his dietary intake of calcium and vitamin D was minimal. He had limited sun exposure. Subsequent PTH was 40 pg/mL (10 - 65 pg/mL) with concurrent serum calcium of 6.5 mg/dL. QTc was prolonged [529 msec (<440 msec)], prompting transfer to the intensive care unit for telemetry, intravenous calcium gluconate, and regular calcium monitoring. Treatment was commenced with cholecalciferol 2000 international units daily and oral calcium carbonate (50 mg elemental calcium/kg/day) in divided doses for presumed Vitamin D deficiency. After several intravenous calcium gluconate doses over 24 hours, the patient’s QTc and ionized calcium normalized. At discharge, calcium was 8.5 mg/dL. He was discharged on the above regimen of calcium and cholecalciferol, and basal and bolus insulin. After discharge, laboratory results returned indicating negative diabetes autoantibodies (GAD 65, Insulin, IA-2) and 25-OH Vitamin D <10 ng/mL (30 - 100ng/mL). Two days after discharge, calcium was 7.3 mg/dL. Two weeks later, labs were: 25-OH Vitamin D 11.3 ng/mL, PTH 10.4 pg/mL, and calcium 9.6 mg/dL. Conclusion: This teen presented with new-onset type 2 diabetes and symptomatic hypocalcemia, an atypical feature of new-onset diabetes. This patient’s hypocalcemia was likely due to both vitamin D deficiency and hypoparathyroidism. He had a low vitamin D level and poor calcium intake with elevated alkaline phosphatase; however, his high normal serum phosphorus and inappropriately normal PTH (instead of elevated in the setting of severe hypocalcemia) indicated a component of hypoparathyroidism. Calcium normalized with detectable 25-OH Vitamin D levels but PTH remained low. Our case highlights the importance of recognizing both that electrolyte abnormalities at diabetes onset may not be directly attributable to diabetes/hyperglycemia and that vitamin D deficiency and hypoparathyroidism may co-exist.

A Prospective Study of Vitamin D Supplement in Thyroidectomy Patients Based on Relative Decline of Parathyroid Hormone

Background: In postthyroidectomy patients, hypocalcemia is the most common complication to prolong hospital stay and decrease patients’ satisfaction. Based on current evidence, it is recommended to supply vitamin D to patients with high risk of developing hypocalcemia. However, how to stratify the risk of patients remains challenging.Aim: We conducted a prospective study to evaluate the effect of vitamin D supplement (calcitriol) on high-risk hypocalcemia patients based on relative decline of parathyroid hormone (RDP).Method: RDP was calculated by the difference between preoperative and postoperative first-day PTH divided by preoperative PTH and presented as percentage. Patients who underwent total thyroidectomy in addition to bilateral central compartment dissection were enrolled prospectively and were divided into two cohorts: Cohort I: patients with RDP ≤70% and Cohort II: patients with RDP >70%. Patients in Cohort I were then randomly assigned to Group A or B, and patients in Cohort II were randomly assigned to Group C or D. All groups received oral calcium, and patients in Groups B and D also received calcitriol. All patients were followed for one year. In the study, standard procedure dictates that only oral calcium is given to patients whose RDP ≤70% and that oral calcium and calcitriol are given to patients whose RDP >70%. Therefore, Cohort I Group A and Cohort II Group D are controls in this study.Results: The incidence of clinical hypocalcemia in Groups A and D (the controls) was 11.0% (10/91), and 17.6% (16/91) required additional intravenous calcium. Of note, no patients developed permanent hypocalcemia. Furthermore, calcitriol supplement did not have significant impact on clinical outcomes between Group A and B in Cohort I. By contrast, calcitriol supplement distinctly improved clinical outcome by comparing Groups C and D (Cohort II), as marked by clinical hypocalcemia, need of requiring intravenous calcium, and long-termed decreased levels of PTH.Conclusion: Supplying calcitriol based on RDP cutoff of 70% may be a wise practice in thyroidectomy patients, and RDP 70% may be a useful predictor to stratify high-risk patients.

Management of hypocalcemia after modified bilateral radical neck dissection followed with total thyroidectomy: a case report

Hypocalcemia is a common complication after total thyroidectomy due to acute hypoparathyroidsm post-surgery. The incident varies from 7%-69% depends on the surgery center. The management is divided based on the onset and symptoms. Carpal-pedal spasm, seizure, bronchospasms are the emergency symptoms of hypocalcemia that require administration of intravenous calcium. However the management of asymptomatic hypocalcemia with oral calcium, vitamin D and hydrochlorothiazide can be difficult due to wide fluctuations of serum calcium and the risks of complication. Hereby we report a 14-year-old girl with hypocalcemia due to hypoparathyroidsm post modified bilateral radical neck dissection and total thyroidectomy. She had papillary thyroid carcinoma and lymph node metastases. After surgery, she developed classic sign of hypocalcemia, numbness in extremities which progressed to cramps. Physical examination revealed chvostek’s sign. Laboratory examination showed critical value of hypocalcemia with normal level of albumin, hypoparathyroidsm and hypovitaminosis D. The initial treatment was started by giving intravenous calcium gluconate 10% and calcitriol. Monitoring level of calcium and phosphate were performed regularly. Calcium level was maintained by giving high dose of elemental calcium, vitamin D3 and hydrochlorothiazide followed.

Intensive calcium monitoring improves outcomes on hungry bone syndrome in hyperparathyroidism

Objectives. Hungry bone syndrome (HBS) is a severe and underdiagnosed complication of parathyroidectomy in the treatment of primary hyperparathyroidism (PHP) and secondary hyper-parathyroidism to chronic kidney disease (SHP-CKD). Methods. A longitudinal study was conducted to compare the postoperative outcomes of patients who developed HBS in two different time frames: before and after implementing a protocol with an intensive electrolytic monitoring and an algorithm regarding electrolytic supplementation. Results. Overall, 77 parathyroidectomies were included. In PHP, a protocol implementation led to an increased admission of patients in the Intermediate Care Unit for intensive electrolytic monitoring (p<0.001) and an increased rate of oral calcium replacement during hospital stay (p=0.013) compared to pre-protocol era. In SHP-CKD, duration of intravenous calcium replacement was reduced (p=0.010). The prevalence of HBS (9.8% in PHP and 58.3% in SHP-CKD) was similar between the two periods, although its diagnosis had an increased trend in PHP since the protocol implementation. None of the diagnosis of HBS was established due to hypocalcemic symptoms in the post-protocol era (contrary to pre-protocol period, p=0.021). Both hypocalcemia length and duration of surgical ward hospitalization were reduced (p=0.047 and p=0.042, respectively). Conclusions. An improved assessment of hyperparathyroidism and a decrease in HBS severity were noted in the post-protocol era. We strongly recommend the implementation of a standardized protocol with an intensive phosphocalcium monitoring in the high-risk patients who undergo parathyroidectomy due to hyperparathyroidism as it improves the health care and management of HBS.

Fahr syndrome associated with post-thyroidectomy hypoparathyroidism

Context: Fahr’s syndrome is a rare disorder characterized by bilateral and symmetrical abnormal calcifications in basal ganglia and cerebral cortex. Those calcified deposits are due to changes in calcium and phosphorus metabolisms that can be caused by endocrine disorders, mitochondrial myopathies, dermatological and infectious diseases. Clinical manifestations may include a variety of extrapyramidal, cerebelar and neuropsychiatric syndromes. Case report: This study describes a 75-year-old female patient that underwent total thyroidectomy in 1985 due to a multinodular goiter and presented postsurgical hypoparathyroidism. The patient missed follow-up apppoointments with Endocrinology and stopped treating her parathyroid condition. Some time later, she presented with change in behavior, drowsiness, paraesthesias, limb spasms and seizures. A CT scan of the brain was performed, showing multiple and extensive calcifications reaching the cerebellar hemispheres, basal ganglia, thalamus and white subcortical substance symmetrically. Laboratory examinations revealed hypocalcemia, hyperphosphatemia, and low parathyroid hormone (PTH) levels. Intravenous calcium gluconate was used to corret the Ca/P dysfunction. Additionally, appropriate antiepileptic drugs for seizures were used. She presented with progressive improvement of symptoms after treatment. Conclusions: This case report demonstrates the importance of post- thyroidectomy follow-up and early recognition of Fahr syndrome’s symptoms, which prevents the progression of neurological conditions.

Use of parathyroid hormone analog (Teriparatide) in patients with chronic hypoparathyroidism after total thyroidectomy: a case report

Background: Hypoparathyroidism and hypocalcemia is a common postoperative complication, after total thyroidectomy due to thyroid cancer. Standard treatment with supplementation of calcium and vitamin D analogs, usually treat this condition. In some patients, hypoparathyroidism is refractory to standard treatment plus intermittent calcium infusions with persistent low serum calcium levels and associated clinical complications. Attempts have been made to add recombinant human parathormone (rhPTH) to the treatment schedule. To our knowledge, this is the first time that we encounter a patient suffering from treatment-refractory postsurgical hypoparathyroidism who was treated with teriparatide. Case presentation: Male (31 years) with postoperative hypoparathyroidism, after total thyroidectomy due to papillary thyroid cancer, several weeks after the surgery still required intermittent intravenous calcium infusions because of tetany symptoms. He had persistent hypocalcemia despite oral treatment with up to 1 ug calcitriol and 4 g calcium per day necessitating additional intravenous administration of calcium gluconate intermittently. This time, Teriparatide treatment was introduced at once daily 50 micrograms (mcg) subcutaneous injection, while doses of calcium and calcitriol were gradually decreased depending on the response of serum total and ionized calcium taken periodically, which resulted in total resolution of hypocalcemia symptoms and the achievement and maintenance of laboratory normocalcaemia in just 5 days. Conclusion: Treatment refractory chronic hypoparathyroidism may be seen in some cases after total thyroidectomy. Furthermore, the use of recombinant human parathyroid hormone analog (Teriparatide) allows for the control of recurrent hypocalcemia reducing the daily dosage of calcium and vitamin D. Finally, regular intravenous calcium administration was no more needed.