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A 62-year-old man experienced metformin-associated lactic acidosis while being treated for type 2 diabetes mellitus. He presented to the emergency department with abdominal pain and sudden bilateral vision loss. The patient had a history of hypertension, type 2 diabetes mellitus, and alcohol use disorder. Laboratory results showed abnormal levels of creatinine, bicarbonate, anion gap, lactate, and serum osmolarity. Treatment with sodium bicarbonate and hemodialysis was initiated, leading to the resolution of metabolic issues and the return of vision. The transient blindness and shock were attributed to metformin-associated lactic acidosis. [Extracted from the article]

An adult man with a history of severe intellectual developmental disorder and behavioral issues was treated with multiple medications, including quetiapine, valproic acid, and zuclopenthixol, but experienced sedation, extrapyramidal side effects, and lack of efficacy. He was then switched to off-label treatment with clozapine, which initially caused hypersalivation but subsided with increased dosage. Throughout 1.5 years of clozapine therapy, the man showed improvements in aggression, body mass index, blood glucose levels, and overall quality of life. Due to these positive outcomes, the decision was made to continue with clozapine therapy. [Extracted from the article]

A 70-year-old woman experienced metformin associated lactic acidosis after taking metformin for type 2 diabetes. She was admitted to the hospital for renal replacement therapy due to acute renal failure. The woman underwent haemodialysis, which rapidly decreased the metformin concentration in her blood and improved her acidosis. After 12 hours, her metformin concentration was considered non-toxic. This case report provides insight into the potential risks and treatment options for metformin intoxication. [Extracted from the article]

A 51-year-old man experienced diabetic ketoacidosis (DKA) while being treated with empagliflozin/metformin for type 2 diabetes mellitus. He presented to the hospital with abdominal pain and mutism, and had a medical history that included epilepsy, schizophrenia, dyslipidemia, benign prostatic hyperplasia, parkinsonism, and type 2 diabetes mellitus. Upon admission, he had hyperglycemia, ketonaemia, metabolic acidaemia, and acute renal injury. It was determined that the DKA was induced by empagliflozin/metformin. [Extracted from the article]

A 45-year-old woman experienced drug toxicity after overdosing on metformin for diabetes. She suffered from convulsive seizures, metformin-associated lactic acidosis (MALA), cardiac arrest, and vasoplegic shock. Despite treatment with epinephrine, norepinephrine, and vasopressin, her condition did not improve. She was given a single dose of IV methylthioninium-chloride (methylene blue) for drug toxicity, which temporarily improved her blood pressure and lactate levels. However, she ultimately died on the 10th day due to vasoplegic shock and MALA caused by metformin toxicity and overdose. [Extracted from the article]

In a retrospective study of 19 patients conducted between 2013-2022, a case was described of a patient with lymphoma who developed lactic acidosis during treatment with metformin. The patient was admitted to the hospital and had elevated lactate levels. Metformin-associated lactic acidosis was confirmed. The study did not provide specific details about the patient's age, sex, indication for metformin use, route of administration, dosage, duration of treatment, or outcome. [Extracted from the article]

A case report published in Reactions Weekly describes a patient who developed paraparesis, or partial paralysis of the lower limbs, while being treated with metformin for type-2 diabetes. The patient experienced spastic paraparesis and weakness in the lower limbs, and brain MRI results indicated metabolic-related lesions. After discontinuing metformin therapy, the patient's symptoms improved. The report suggests that the paraparesis was a result of metformin treatment, although the duration of treatment to reaction onset was not specified. [Extracted from the article]

This article discusses two cases of encephalopathy and lactic acidosis associated with the use of metformin, a medication commonly used to treat diabetes mellitus. In the first case, a 55-year-old man developed these complications while taking metformin for diabetes, despite receiving dialysis treatment. The second case involves a 58-year-old man who experienced encephalopathy and lactic acidosis due to a medication error, where he was unintentionally prescribed metformin. Both patients showed improvement after discontinuing metformin and undergoing hemodialysis. The article emphasizes the importance of monitoring patients on metformin, especially those with kidney disease, to prevent such complications. [Extracted from the article]

In a retrospective case control study, three male patients with type 2 diabetes mellitus were found to have a lack of efficacy when treated with metformin, insulin-aspart, insulin-glargine, or insulin-aspart/insulin-protamine-aspart. These patients were also diagnosed with head and neck squamous cell carcinoma and received chemoradiotherapy with cisplatin. Despite the treatment, they developed diabetes-related complications and required hospitalization. Two patients required enteral feeding with insulin, while one patient continued receiving metformin and insulin. [Extracted from the article]

A case report published in the journal Reactions Weekly describes a 55-year-old man with type 2 diabetes mellitus who exhibited a lack of efficacy during treatment with metformin. The patient had a diabetic foot ulcer and neuropathy and had been taking metformin for two years. Despite treatment, his hemoglobin A1C levels increased and his fasting blood sugar levels remained high, indicating a lack of effectiveness of metformin in controlling his diabetes. The report highlights the need for alternative treatment options for patients who do not respond well to metformin. [Extracted from the article]

A 52-year-old woman with diabetes and chronic kidney disease developed metformin-associated lactic acidosis after consuming expired canned food. She presented with altered mental status, hypotension, and tachycardia, and was admitted to the ICU. Investigations revealed a serum lactate level of 10.7 mmol/L, which increased to 31.8 mmol/L in less than 12 hours. Blood, tracheal, and stool cultures were positive for Salmonella Infantis, indicating concurrent septic shock with multiorgan failure. The woman was treated with pressors, continuous renal replacement therapy, antibiotics, bicarbonate drip, and insulin drip, and eventually showed clinical improvement. Her metformin level was found to be elevated, and the medication was discontinued. [Extracted from the article]

A 21-year-old woman with diabetes experienced a lack of efficacy and skin swelling at the injection site while being treated with insulin-lispro, insulin-glargine, and metformin. Despite receiving therapy, her diabetes was not controlled, and she developed skin swelling associated with the insulin injections. Further investigation revealed a genetic variant that led to a diagnosis of maturity onset diabetes of the young (MODY). Treatment with a sulfonylurea improved her diabetes control, and the insulin dose was decreased with the goal of discontinuing it once her blood sugars were at the desired level. [Extracted from the article]

In a case series, two 16-year-old girls were described who experienced lack of efficacy with various drugs used to treat hyperglycemia. The first girl had LMNA-associated severe insulin resistance syndrome and was treated with insulin, metformin, pioglitazone, saxagliptin, and unspecified thiazolidinediones and dipeptidyl-peptidase-4-inhibitors, but her hyperglycemia did not improve until dapagliflozin was added. The second girl had PIK3R1-associated severe insulin resistance syndrome and intentionally stopped taking dapagliflozin, resulting in worsening hyperglycemia. These cases highlight the challenges of managing hyperglycemia and the importance of individualized treatment approaches. [Extracted from the article]

A retrospective chart review of 38 patients conducted between 1991 and 2022 described a 58-year-old woman who developed apparent sporadic chorea (ASC) while being treated with metformin for type 2 diabetes mellitus. The woman, who had renal failure, started receiving metformin treatment and subsequently developed ASC as a result. The specific details regarding the route, dosage, duration of treatment, and outcome were not provided in the article. [Extracted from the article]

A 61-year-old woman experienced various toxicities, including high anion gap metabolic acidosis (HAGMA), lactic acidosis, nausea, vomiting, and drug toxicity, while being treated with paracetamol, ketamine, and metformin for sciatica and diabetes mellitus. The woman had pre-existing conditions such as chronic kidney disease, hypertension, arthritis, and diabetes mellitus. She was hospitalized after developing altered mental status, hypoglycemia, and hypotension. Despite resuscitation efforts, she experienced cardiac arrest and ultimately died. The toxicities were attributed to metformin toxicity, paracetamol, and ketamine therapies, and were responsible for the woman's renal failure, anoxic brain injury, cardiogenic shock, and cardiac arrest. [Extracted from the article]

An 8-year-old boy developed lactic acidosis during anesthesia treatment with propofol and sevoflurane. The boy was undergoing surgery for Perthes' disease and received propofol, rocuronium-bromide, fentanyl, and sevoflurane. He experienced lactic acidosis postoperatively, which was attributed to the use of propofol and sevoflurane. In a subsequent surgery, the boy received different medications and did not experience lactic acidosis. He was discharged from the hospital without any further complications. [Extracted from the article]

A 12-year-old girl with type 2 diabetes, autoimmune thyroid disease, and obesity experienced a lack of efficacy during treatment with insulin, metformin, and levothyroxine sodium. She presented with recurrent nosebleeds and was subsequently diagnosed with metabolic syndrome. Despite receiving treatment, her condition worsened, indicating a lack of effectiveness of the medications. [Extracted from the article]

A 26-year-old woman with type 2 diabetes and hypertension intentionally overdosed on lisinopril and metformin, resulting in lactic acidosis and shock. Despite treatment with various medications, including norepinephrine and methylthioninium-chloride, her condition did not improve. She ultimately underwent kidney replacement therapy and her condition resolved, with her kidney function returning to normal. [Extracted from the article]

A 67-year-old man with a medical history of HIV infection developed lactic acidosis after receiving an extra dose of bictegravir/emtricitabine/tenofovir-alafenamide, a medication for HIV. He was admitted to the hospital with general weakness and was diagnosed with septic shock. Laboratory tests revealed metabolic acidosis and elevated lactic acid levels. It was discovered that the man had been taking twice the recommended daily dose of the medication due to a medication error. After discontinuing the medication and receiving treatment, his lactic acidosis resolved and he was discharged from the hospital. [Extracted from the article]

A 67-year-old woman experienced lactic-acidosis while being treated with salbutamol for a respiratory infection. She was admitted to the hospital with SARS-CoV-2 pneumonia and a bacterial respiratory infection. The medical team provided emergency and acute care, including mechanical ventilation, within the first 24 hours of her admission. After starting treatment with inhaled salbutamol, she developed lactacidemia. Other potential causes of cellular hypoxia were ruled out, and salbutamol was discontinued. As a result, her lactate levels returned to normal. [Extracted from the article]

A 73-year-old man with type-2 diabetes mellitus experienced lack of efficacy while taking dapagliflozin, metformin, and vildagliptin. He subsequently developed hypernatraemia, metabolic acidosis, and metabolic alkalosis during treatment with bicarbonate, as well as normoglycaemic ketoacidosis while taking dapagliflozin. The man was admitted to the emergency department with symptoms including malaise, bilious vomiting, and refusal to eat. Treatment with insulin resolved the normoglycaemic ketoacidosis and metabolic acidosis. [Extracted from the article]

A 19-year-old woman developed lactic acidosis while being treated with methylprednisolone for acute spinal cord injury. She was hospitalized after a fall and underwent surgical fixation of a fracture. During her treatment, she received phenylephrine and fluid resuscitation, as well as a bolus dose and infusion of methylprednisolone. Shortly after starting methylprednisolone, her lactate levels increased, indicating hyperlactatemia. The lactic acidosis was determined to be a type B reaction to the methylprednisolone. The duration of treatment and outcome were not specified. [Extracted from the article]

A 54-year-old woman was hospitalized in the ICU after intentionally overdosing on several medications, including a large amount of metformin, for depression. She experienced severe lactic acidosis, characterized by low pH and high lactate levels, as a result of the metformin overdose. The woman received various treatments, including mechanical ventilation, activated charcoal, glucose, fluid, aminergic support, and continuous venovenous hemofiltration (CVVHF). With the high dialysis dose and CVVHF, her condition improved, and she eventually recovered from the severe lactic acidosis. [Extracted from the article]

In this case report from Reactions Weekly, two patients with type-2 diabetes mellitus developed metformin toxicity, leading to metformin associated lactic acidosis. The first patient, a 62-year-old man, was hospitalized with dizziness and vomiting. The second patient, a 45-year-old woman with metastatic breast cancer, presented with encephalopathy. Both patients were treated and their metformin toxicity and lactic acidosis resolved. The report highlights the potential risks associated with metformin use in certain individuals. [Extracted from the article]

A 63-year-old woman with type II diabetes mellitus and chronic kidney disease developed drug toxicity in the form of an elevated metformin blood level. She had received IV contrast for abdominal pain prior to her presentation, and her laboratory tests revealed severe lactic acidosis. The woman underwent haemodialysis and her metformin level in blood was found to be elevated. The drug toxicity and lactic acidosis were considered secondary to the elevated metformin blood level, and her condition improved after haemodialysis. [Extracted from the article]

A 70-year-old woman experienced euglycemic diabetic ketoacidosis while being treated with empagliflozin and metformin for type 2 diabetes. She also showed a lack of effectiveness when treated with sodium bicarbonate for acidosis. The woman was admitted to the hospital due to severe diarrhea and presented with low blood pressure, high glucose levels, and abnormal blood test results. Despite initial treatment with sodium bicarbonate, her condition worsened, and she was ultimately diagnosed with euglycemic diabetic ketoacidosis and acute kidney injury. However, after receiving hydration, insulin, and hemodialysis, her condition improved. [Extracted from the article]

A 67-year-old woman experienced lactic-acidosis while being treated with salbutamol for a respiratory infection. She was initially admitted with SARS-CoV-2 pneumonia and a bacterial respiratory infection. The medical team provided emergency and acute care, including mechanical ventilation, within the first 24 hours of her admission. After starting treatment with inhaled salbutamol, she developed lactacidemia. Other potential causes of cellular hypoxia were ruled out, and once salbutamol was discontinued, her lactate levels returned to normal. [Extracted from the article]

A 73-year-old man with type-2 diabetes mellitus experienced lack of efficacy while taking dapagliflozin, metformin, and vildagliptin. He subsequently developed hypernatraemia, metabolic acidosis, and metabolic alkalosis during treatment with bicarbonate, as well as normoglycaemic ketoacidosis while taking dapagliflozin. The man was admitted to the emergency department with symptoms including malaise, bilious vomiting, and refusal to eat. Treatment with insulin resolved the normoglycaemic ketoacidosis and metabolic acidosis. [Extracted from the article]

A 63-year-old woman with type II diabetes mellitus and chronic kidney disease developed drug toxicity in the form of an elevated metformin blood level. She was referred for acute kidney injury and severe lactic acidosis, which was suspected to be caused by metformin toxicity. The woman underwent haemodialysis and her condition improved. The elevated metformin blood level was considered to be the cause of the drug toxicity. [Extracted from the article]

In this case report from Reactions Weekly, two patients with type-2 diabetes mellitus developed metformin toxicity, leading to metformin associated lactic acidosis. The first patient, a 62-year-old man, was hospitalized with dizziness and vomiting. The second patient, a 45-year-old woman with metastatic breast cancer, presented with encephalopathy. Both patients were treated and their metformin toxicity and lactic acidosis resolved. The report highlights the potential risks associated with metformin use and the importance of monitoring for toxicity. [Extracted from the article]

A 54-year-old woman was hospitalized in the ICU after intentionally overdosing on several medications, including a large amount of metformin, for depression. She experienced severe lactic acidosis, characterized by low pH and high lactate levels, as a result of the metformin overdose. The woman received various treatments, including mechanical ventilation, activated charcoal, glucose, fluid, aminergic support, and continuous venovenous hemofiltration (CVVHF). With the high dialysis dose and CVVHF, her condition improved, and she eventually recovered from the severe lactic acidosis. [Extracted from the article]

A 19-year-old woman developed lactic acidosis while being treated with methylprednisolone for acute spinal cord injury. She was hospitalized after a fall and underwent surgical fixation of a fracture. During her treatment, she received phenylephrine and fluid resuscitation, as well as a bolus dose and infusion of methylprednisolone. Shortly after starting methylprednisolone, her lactate levels increased, indicating hyperlactatemia. The lactic acidosis was determined to be a type B reaction to the methylprednisolone. The duration of treatment and outcome were not specified. [Extracted from the article]

A 70-year-old woman experienced euglycemic diabetic ketoacidosis while being treated with empagliflozin and metformin for type 2 diabetes. She also showed a lack of effectiveness when treated with sodium bicarbonate for acidosis. The woman was admitted to the hospital due to severe diarrhea and presented with low blood pressure, high glucose levels, and abnormal blood test results. Despite treatment with sodium bicarbonate, her condition worsened, and she was eventually diagnosed with euglycemic diabetic ketoacidosis and acute kidney injury. However, after receiving hydration, insulin, and hemodialysis, her condition improved. [Extracted from the article]

A 52-year-old man experienced diabetic ketoacidosis while being treated with dapagliflozin for type 2 diabetes mellitus. He also showed a lack of efficacy when treated with metformin and semaglutide for the same condition. The man had a history of diabetes, hypertension, and hyperlipidemia, and presented to the emergency department with symptoms including shortness of breath, nausea, abdominal pain, and increased thirst and urination. He was diagnosed with diabetic ketoacidosis and treated with insulin infusion. After discontinuing dapagliflozin, he was discharged on a basal-bolus insulin regimen. However, during a follow-up visit, his hemoglobin A1C levels increased, indicating a lack of efficacy with metformin and semaglutide, and he was restarted on insulin therapy. [Extracted from the article]

A 52-year-old man experienced diabetic ketoacidosis while being treated with dapagliflozin for type 2 diabetes mellitus. He also showed lack of efficacy when treated with metformin and semaglutide for the same condition. The man had a history of diabetes, hypertension, and hyperlipidemia, and presented to the emergency department with symptoms including shortness of breath, nausea, abdominal pain, and increased thirst and urination. He was diagnosed with diabetic ketoacidosis and treated with insulin infusion. After discontinuing dapagliflozin, he was discharged on a basal-bolus insulin regimen. However, his hemoglobin A1C levels increased when he transitioned to metformin and semaglutide, and he was restarted on insulin therapy. [Extracted from the article]

A 58-year-old man with type 2 diabetes mellitus developed lactic acidosis, myalgia, and muscle tension while being treated with metformin. The patient's muscle specimen showed abnormal accumulation of mitochondria and lipid vacuoles. After discontinuing metformin, the patient's serum lactate level decreased significantly. This case highlights the potential side effects of metformin treatment for diabetes. [Extracted from the article]

This article discusses two cases of lactic acidosis, a serious condition, in elderly women who were being treated for type 2 diabetes mellitus. In the first case, a 76-year-old woman developed lactic acidosis while taking metformin. She was treated with fluid infusion, sodium bicarbonate, and dialysis, and eventually recovered. In the second case, a 78-year-old woman developed lactic acidosis while taking sodium bicarbonate for the condition. Despite treatment with sodium bicarbonate and dialysis, her lactate levels continued to rise, but she eventually recovered after receiving additional treatment for acute renal failure. [Extracted from the article]

A 70-year-old woman experienced lactic-acidosis while being treated with metformin for diabetes and also showed lack of efficacy when treated with sodium bicarbonate for lactic-acidosis. The woman had a history of hypertension and diabetes and had been hospitalized multiple times in the past due to acute kidney injury. On admission, her condition worsened despite treatment with sodium bicarbonate, but her lactic acidosis resolved within 24 hours after receiving continuous renal replacement therapy. She discontinued the use of metformin. [Extracted from the article]

A retrospective study examined 107 patients who developed metformin-associated lactic acidosis (MALA) following metformin intoxication. The study included 19 patients aged 44-89 years, with acute kidney injury, chronic kidney disease, shock, or end-stage renal disease. The patients were hospitalized and had elevated serum metformin levels. Treatment interventions included ventilatory support, vasopressor support, and renal replacement therapy. Unfortunately, seven patients died from MALA. [Extracted from the article]

A 68-year-old man experienced metabolic acidosis and vision loss while being treated with metformin for diabetes mellitus. The man had a history of diabetes and was also taking glibenclamide and sitagliptin. After traveling to Tanzania, he developed severe pain in his lower limbs and returned to India. He was hospitalized and found to have significant renal dysfunction. Following dialysis, he suddenly lost vision in both eyes, but his vision gradually improved after receiving treatment in the ICU. The man's metabolic acidosis was corrected, and further tests revealed positive urine myoglobin and elevated creatine phosphokinase levels. [Extracted from the article]

A 79-year-old woman with end-stage renal disease and type 2 diabetes developed lactic acidosis while being treated with metformin. She presented to the emergency department with altered mental status and was found to be hypoglycemic. Laboratory results confirmed lactic acidosis, and she was diagnosed with this condition as a result of metformin use. The woman was treated with dialysis and her symptoms resolved, leading to her discharge from the hospital on day 3. [Extracted from the article]

A 59-year-old man experienced a lack of efficacy while being treated with hydrochlorothiazide for hypertension. He had a history of well-controlled type 2 diabetes mellitus, hypertension, and hyperlipidemia. The man's blood glucose level became elevated, and he experienced symptoms such as polyuria, polydipsia, and increased fatigue. Despite taking antihypertensive medication, his blood pressure was not controlled, indicating a lack of efficacy of hydrochlorothiazide. The medication was discontinued, and he was prescribed prazosin instead. After undergoing a right adrenalectomy for pheochromocytoma, his condition improved and his medication doses were adjusted accordingly. [Extracted from the article]

A 36-year-old man with maternally inherited diabetes and deafness (MIDD) experienced a lack of efficacy while being treated with glipizide, linagliptin, and metformin. Despite receiving these medications, his glycemic control remained poor. Glipizide was discontinued, and he was switched to basal insulin and sitagliptin, which resulted in improved glycemic control. He also received empagliflozin and later empagliflozin/linagliptin to reduce the number of pills he had to take. Over a period of 3 years, his HbA1c levels remained at 6.5% or lower, and there was an improvement in his MIDD. [Extracted from the article]

A 43-year-old woman with type 2 diabetes mellitus developed high anion-gap metabolic acidosis and non-anion-gap metabolic acidosis while being treated with metformin and sodium-glucose-transporter-2 (SGLT2) inhibitors. She experienced symptoms such as nausea, dizziness, malaise, dyspnea, vomiting, and palpitations. Laboratory tests revealed respiratory alkalosis, mixed anion-gap and non-anion-gap metabolic acidosis, and euglycemic diabetic ketoacidosis. The woman was treated with IV fluids, insulin drip, and bicarbonate therapy, and eventually recovered. The SGLT2 inhibitors were discontinued, but she continued treatment with metformin and pioglitazone. [Extracted from the article]

A 42-year-old woman with type 2 diabetes mellitus exhibited lack of efficacy during treatment with metformin. Despite taking metformin, her glucose levels and symptoms did not improve. Further investigation revealed that she had pheochromocytoma, a rare tumor that affects the adrenal glands. The woman was then started on insulin, doxazosin, and amlodipine, and underwent a successful surgery to remove the tumor. After the surgery, her glucose levels and symptoms significantly improved. [Extracted from the article]

A 65-year-old woman with a medical history of morbid obesity, hypertension, and type 2 diabetes developed hyperosmolar hyperglycemic state while being treated with semaglutide. She also had drug intolerance with metformin and stopped taking it after one week. The woman presented with altered mental status, progressive abdominal pain, nausea, vomiting, and weight loss. Her blood glucose levels were extremely high, and she had other abnormal laboratory findings. The likely cause of her condition was the management of her newly diagnosed diabetes with semaglutide. [Extracted from the article]

A 34-year-old woman with a family history of diabetes was diagnosed with latent autoimmune diabetes (LADA) in adults. She initially managed her diabetes with diet control and lifestyle changes, but her hyperglycemia persisted. She was prescribed metformin and gliclazide, but these medications also proved ineffective. Sitagliptin was added to her treatment regimen, but it did not improve her condition either. She experienced weight loss and was eventually diagnosed with LADA. Her treatment was changed to insulin therapy, and her condition improved with time. [Extracted from the article]

A 60-year-old woman experienced hypoglycemia and developed hemichorea (involuntary movements) while being treated with glimepiride/metformin for diabetes mellitus. The woman had a low body mass index and irregular diet, which were considered contributing factors to the hypoglycemia. She was admitted to the hospital, where her medication dosage was adjusted and she was treated with glucose and haloperidol. Her symptoms improved, and she was discharged with instructions for regular blood sugar monitoring. Follow-up MRI scans showed a reduction in abnormal brain signals. [Extracted from the article]

A 60-year-old man with a history of diabetes mellitus and diabetic neuropathy developed diabetic ketoacidosis and lactic acidosis while being treated with empagliflozin, metformin, and insulin. He presented to the emergency room with symptoms of malaise, vomiting, abdominal pain, and dizziness. The man had been non-compliant with his insulin treatment. He was treated with IV fluids, antibiotics, insulin, and generous fluid resuscitation. His lactic acidosis and creatinine levels improved, and he was discharged after adjusting his insulin regimen and discontinuing empagliflozin. [Extracted from the article]

A 53-year-old man experienced lack of efficacy while being treated with metformin for diabetes, methotrexate for ankylosing spondylitis, monascus for hyperlipidemia, clindamycin for a pressure injury infection, and amobarbital for fever. He also self-administered metformin and monascus, indicating drug misuse. The man had a history of car accident injuries, including a fracture and dislocation of the cervical spine, and had been bedridden for a long time. Despite various treatments, including antibiotics and wound debridement, his condition continued to deteriorate. Eventually, his pressure injury area improved and he was discharged from the hospital. [Extracted from the article]