In KWNP, compression of the contralateral cerebral peduncle in a subdural hematoma can damage the descending corticospinal tract and subsequently cause ipsilateral hemiparesis. There can be wide variability in the morphology of this pathology [3]. Thus, it is important to differentiate KWNP from other etiologies of ipsilateral hemiparesis like cerebrovascular dysfunction of the contralateral hemisphere or mass effect from cerebral neoplasms. Our postoperative studies did not provide clinical evidence in support of an ischemic stroke or malignancy.

KWNP is rarely reported in the literature especially in young women and in patients with heavy alcohol use. A systematic review of English-language articles containing KWNP found that the mean age of presentation was 40.7 years old and the male/female sex ratio was 2:1. Interestingly, in previous studies, the mechanism behind KWNP seemed to primarily arise from head trauma (e.g., blunt trauma, falls, car crashes, etc.) [4]. In our patient, the historian denied any trauma to the head and the physical exam did not reveal any contusions or evidence of trauma. Additionally, only one other study emerged that demonstrated KWNP in a patient with a history of alcohol abuse [5]. It has been well-documented that alcohol use is a risk factor for acute and chronic subdural hematoma [1, 6]. Further investigation into the link between chronic alcohol use and the presence of KWNP could be warranted in future studies.

Another incidental finding in our case report was the delayed emergence of delirium tremens. In our patient, the constellation of symptoms associated with delirium tremens (e.g., autonomic dysfunction, agitation, acute coronary syndrome) occurred on POD #6. Delirium tremens are typically seen between 48 and 96 h after a patient ceases ingestion of ethanol [7]. The phenomenon is already rare: about 50% of patients with alcohol use disorder will develop alcohol withdrawal syndrome and about 3% to 5% of those patients will develop delirium tremens [8]. Due to the short-acting nature of ethanol, withdrawal symptoms typically begin within 8 h after blood alcohol levels start to decrease. These symptoms peak at approximately 72 h. The symptoms tend to abate by 120 h [9, 10]. In our patient, the autonomic hyperactivity, psychomotor agitation, and coronary sequelae of delirium tremens started approximately at 144 h. This incidental finding was hypothesized to be due to the patient being extubated on POD #3. There is a lack of research documenting the time course of delirium tremens in patients who were intubated. Future studies and case reports may provide further insight into how intubation may delay the emergence of delirium tremens.

By ruling out cerebrovascular dysfunction, ischemic stroke, and structural abnormalities, our case report strengthens the differential diagnosis of KWNP in a patient with paradoxical ipsilateral hemiparesis. This report also contributes to the existing literature that associates subdural hematomas with KWNP. Our presentation provides an uncommon demographic of KWNP (e.g., a young woman) in the setting of chronic alcohol use with severe complications. It is worth noting that we did not obtain ancillary studies such as coronal views of the MRI, diffusion tensor imaging, or motor-evoked potentials. These have previously been reported to visualize KWNP in the literature [11].

Additionally, our report illustrates a case of late delirium tremens. Given the significant morbidity linked with delirium tremens and its varied presentation, this report could guide future diagnostic protocols for identifying delirium tremens. Subsequent research could explore the underlying pathophysiology contributing to the delay in the onset of delirium tremens, potentially attributed to intubation.

This case underscores the importance of considering KWNP in cases of paradoxical ipsilateral hemiparesis associated with subdural hematomas, especially in young individuals with heavy alcohol use. Early detection of KWNP could lead to refined diagnostic algorithms and advance our understanding of this rare phenomenon. The case report provides an alternative method to rule out other possible etiologies of ipsilateral hemiparesis through imaging studies when characteristic features of the disease are not easily located. Further research is needed to uncover its underlying mechanisms and risk factors.