Central Diabetes Insipidus State Following Laparoscopic Surgery with Hiatal Hernia Repair
Corresponding author: Dr. Meng-Feng Wu, Taoyuan Armed Forces General Hospital, No. 168, zhongxing Rd, Longtan Dist, Taoyuan city, Taiwan, Tel: 8863479959#326852; Email: firstname.lastname@example.org
Hiatal hernias are a common finding on radiographic or en- doscopic studies. Laparoscopic surgery was found to be effec- tive for the problem. However, it had not been reported that cormobility of idiopathic central diabetes insipidus(CDI). The exact mechanism of its occurrence is also unknown. The pur- pose of reporting this case is to highlight the importance of anticipation and early recognition of CDI in patient postoper- atively with an aim to intervene as soon as possible and avoid neurological damage and cerebral edema. This is the first case in which hiatal hernia status post-surgery accompanied by central diabetes that was managed successfully.
A 36-year-old male was referred to our department because of sliding hiatal hernia detected on chest computed tomogra- phy(Fig.1A) and underwent the pan endoscopy by the astrol- ogist(Fig.1B). Failed the conservative treatment with proton pump inhibitor and symptom of easily vomiting and heart
physical examination and laboratory work-up were within normal limits. He has no other medical issues and has no pri- or abdominal surgery. He underwent the laparoscopic surgery with hiatal hernia repair and Nissen fundoplication. (Fig2A). However, post-operative polyuria (daily urine output:7710ml) and hypernatremia (190 mmol/L) developed. Suspicious of diagnosis of central diabetes insipidus, we consulted the ne- phrologist and endocrinologist and administered the desmo- pressin(dDAVP) agent and closely monitoring and the cor- rection of plasma sodium (falling by 1 mmol/L per hour) to avoid the convulsions and cerebral edema. Sub sequentially, myalgias, weakness, red to brown urine and rhabdomyolysis also developed (Creatine kinase :42900u/L). We administered adequate fluid resuscitation, and alkalization of the urine to avoid the acute kidney injury and disseminated intravascular coagulation and compartment syndrome. After a series of cor- rection, extubation of endotracheal tube successfully and the patient was transferred to ordinary ward. After discharged, he visited our outpatient department with the examination brain magnetic resonance imaging (MRI) of sella study. There is no evidence of focal lesion of the pituitary gland that is either
non-enhanced or delay enhanced during the dynamic perfu- sion study or delayed phase images. Dynamic esophagogram with barium contrast also had done and patent of the esoph- agus lumen without stricture(Fig2B). There was no complica- tion with 3-month interval follow up.
Hiatus hernias are a protrusion of intra-abdominal contents into the thoracic cavity via a defect in the diaphragmatic hi- atus. They are classified into four different subtypes: type I (sliding hiatal hernia) and types II, III, IV which refer to parae- sophageal hernias of increasing severity . In type I hernias, the gastroesophageal junction (GOJ) moves into the posterior mediastinum via the esophageal hiatus without forming a her- nia sac . These hernias are rarely asymptomatic; causing dysphagia, chest pain, reflux and postprandial fullness .
The patient remained symptomatic for a long period of time and presented in easy vomiting and chest pain even conserva- tive medicine with proton pump inhabitor agent administra- tion.and life style change. The principal management includes reduction of abdominal contents and repairing the defect to prevent life threatening complications. Approach via laparos- copy given its favorable outcomes and recovery profiles .
The present case was diagnosed with subclinical diabetes in- sipidus of the central type, which was not evident after lapa- roscopic surgery. He experienced similar symptoms, such as polyuria and polydipsia. Thus, surgery might have been an ag- gravating factor for the development of overt central diabetes insipidus(CDI). Although the causal linkage between diabetes insipidus and hiatal hernia repair remains unclear, several studies have speculated an underlying mechanism for this as- sociation [1,4,5]. CDI may be caused by CNS neoplasms (25%), neurosurgery (20%) and head trauma (16%) and granuloma- tous diseases (<5%) (5). In up to 30% of the cases, the etiology remains unknown (idiopathic)  We searched Pub Med and could not find any case records.
CDI is diagnosed by means of the water deprivation test and response to desmopressin . The former was technically not possible in our patient as she was on a ventilator. The very high serum sodium levels and low urine osmolality were indicative of diabetes insipidus (DI) as the culprit disorder. Our patient responded to desmopressin with an almost 50% reduction of her urine output, which supported the diagnosis of CDI; The treatment of CDI involves decreasing the urine output by in- creasing the activity of ADH. In addition, replacement of on- going volume losses and correction of hypernatremia is es- sential. Desmopressin (dDAVP) is the preferred treatment . The hypernatremia was also treated, by calculating the “water deficit” and replacing it to cautiously correct sodium levels to
<10 meq/day. The fluid used was 5% dextrose in water, while initially one-liter bolus of normal saline was used when the pa- tient was in shock.
Extreme hypernatremia (>190 mmol/L) is rare, and only a few cases have been reported. Borrego et al Studied  pa-
tients with extreme hypernatremia>190 mmol/dL from 1990 to 2003. There were 26 patients with sodium levels ranging from 190 to 274 mmol/L. Mortality was 41% and 67% in children and adults, respectively. The most common cause of mortality in adults was the use of saline emetics. Wrong for- mula concentration was the most common cause in neonates. There was no teenage group like our patient reported to have such a high serum sodium level.
Rhabdomyolysis has early and late complications. Cell lysis in- duces hyperkalemia and hypocalcemia, and increases the im- mediate risk of cardiac arrest. Twenty-five percent of patients have impaired liver function. The most serious complication is ARF, which usually occurs in the initial 12–24 hours after muscle injury. The pathogenesis of ARF includes mechanical obstruction of tubules by myoglobin, direct toxic effect of free cheatable iron on tubules, and hypo perfusion of the kidneys. Patients are at higher risk if creatine kinase level is >16,000 U/L . Fortunately, rhabdomyolysis and the consequent ARF can be completely resolved with early adequate hydration and alkalization. Most renal functions improve within days to 1–2 months.
Figure 1A: The stomach and the section of the esophagus that joins the stomach slide up into the chest through the hiatus
Figure 1B: Panendoscopic finding is Loose Eeophagogas- tric junction and mucosal breaks over eeophagogastric junction
<5mm, diffuse gastrointestinal hemorrhage pattern
Figure 2A: Perioperative repairing the hiatus and hanging the esophagus and Nissen fundoplication
Figure 2B: Patent of the esophagus lumen and passage of oral contrast is smooth without Stricture postoperatively
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