Programmable shunt valves have become a valuable tool in hydrocephalus management. The option to non-invasively change valve settings has been reported as advantageous over conventional fixed valves during management of NPH, hydrocephalus, chronic SDH, SDH and ventricular collapse due to over-drainage, and preventing SDH recurrence following evacuation [2
]. The Dutch Normal-Pressure Hydrocephalus study showed that 71 percent of patients with fixed low-pressure valves developed subdural effusions compared to 34 percent for patients with fixed medium-pressure valves [3
]. Thus, the development of subdural effusions seems to be directly related to the amount of CSF drainage.
Adjustable valves not only provide the ability to non-surgically increase valve settings to prevent subdural effusions, but also provide the added benefit of high-pressure drainage when needed to aid in the treatment of subdural effusions. Carmel et al
. reported the use of shunt ligation and high-pressure drainage to treat a subdural fluid collection in a patient with NPH. Initially, shunt ligation was performed on a patient in an attempt to obliterate the subdural fluid collection, which unfortunately resulted in rapid deterioration of the patient. Due to worsening of patient’s clinical condition, the ligature was removed and the adjustable valve turned to a high-pressure setting. The adjustable valve provided the safety of high-pressure drainage, and the patient returned to baseline over five days [4
Sindou et al
. also reported on the treatment options offered by adjustable valves; in a series of 75 patients, 27 patients required non-operative valve adjustment to address hemispheric detachment, intracranial hypotension and absence of clinical improvement [13
]. The benefit of adjustable shunts are further reinforced in a report by Zemack et al
., which concluded that non-invasive shunt adjustment improved outcomes for patients with NPH after reporting a five-year adjustable shunt survival rate of 80.2 percent, with good to excellent outcomes observed in 78.1 percent of people with idiopathic NPH [14
The literature has demonstrated benefit in lowering the incidence and treating chronic subdural hematomas in patients with NPH with adjustable shunt valve placement. However, there is very scant literature describing acute SDH management in shunted patients with NPH. This is surprising as the development of acute SDH after shunting for NPH is a serious concern. Even minor head trauma may lead to an acute SDH, necessitating surgical intervention [9
]. Increased susceptibility to SDH can be attributed to the shunt decreasing intracranial pressure by decreasing ventricular volume, causing the vessels bridging the subdural space to become stretched and making them vulnerable to sheering forces and bleeding upon minor trauma [8
]. Once bleeding begins, the ventricular shunt facilitates hematoma development by preventing the brain from tamponading further bleeding [15
]. Furthermore, SDH development have been attributed to over-drainage of CSF alone, highlighting the strain experienced by subdural bridging vessels in patients with ventriculoperitoneal shunts [2
Hoya et al
. reported one case of non-operative acute SDH management in a patient with normal-pressure hydrocephalus and an adjustable valve [6
]. They adjusted the valve to the highest setting in order to decrease CSF drainage. This patient unfortunately died from complications that appeared to be unrelated to the subdural hematoma. Hoya’s results are in contrast with the case that we present. Our patient was readmitted after six days following issues of NPH symptoms, including gait ataxia, generalized weakness and urinary incontinence. A CT of the head obtained upon readmission revealed complete resolution of the acute SDH and not just a reduction in volume. The valve pressure was then reduced to treat the NPH symptoms, and our patient’s neurological condition improved upon discharge. To the best of our knowledge, this is the first case detailing the results of non-operative shunt valve management of an acute SDH.