The Magnitude of Postconvulsive Leukocytosis Mirrors the Severity of Periconvulsive Respiratory Compromise: A Single Center Retrospective Study

Abstract

Background: Generalized epileptic convulsions frequently exhibit transient respiratory symptoms and non-infectious leukocytosis. While these peri-ictal effects appear to arise independently from one another, the possibility that they stem from a common ictal pathophysiological response has yet to be explored. We aimed to investigate whether peri-ictal respiratory symptoms and postictal leukocytosis coexist.Methods: We performed a single center retrospective chart review of 446 patients brought to our emergency department between January 1, 2017 and August 23, 2018 for the care of generalized epileptic convulsions with or without status epilepticus. We included 152 patients who were stratified based on the presence (PeCRC+) or absence (PeCRC–) of overt periconvulsive respiratory compromise (PeCRC). In addition, patients were stratified based on the presence or absence of postconvulsive leukocytosis (PoCL), defined as an initial postconvulsive white blood cell (WBC) count ≥ 11,000 cells/mm3. Triage vital signs, and chest x ray (CXR) abnormalities were also examined.Results: Overt PeCRC was observed in 31.6% of patients, 43% of whom required emergent endotracheal intubations. PoCL was observed in 37.5% of patients, and was more likely to occur in PeCRC+ than in PeCRC– patients (79.2 vs. 18.2%; OR = 17.0; 95% CI = 7.2–40.9; p < 0.001). Notably, the magnitude of PoCL was proportional to the severity of PeCRC, as the postconvulsive WBC count demonstrated a negative correlation with triage hemoglobin oxygen saturation (R = −0.22; p < 0.01; CI = −0.48 to −0.07). Moreover, a receiver operating characteristic analysis of the WBC count's performance as predictor of endotracheal intubation reached a significant area under the curve value of 0.81 (95% CI = 0.71–0.90; p < 0.001). Finally, PeCRC+ patients demonstrated frequent CXR abnormalities, and their postconvulsive WBC counts correlated directly with triage heart rate (R = 0.53; p < 0.001).Conclusion: Our data support the existence of an ictal pathophysiological response, which induces proportional degrees of PoCL and PeCRC. We suggest this response is at least partially propelled by systemic catecholamines.

Recurrent cerebellar ischemic infarctions and stereotyped peri-ictal sympathetic responses in a near-SUDEP patient with cardiovascular risk factors

“… [10] Considering our patient’s unfavorable outcome, these data suggest a potential association between postictal troponin elevations and clinically severe GTCSs. A similar conclusion can be reached about frank postictal leukocytoses (i.e., leukocyte elevations beyond the normal range) as uncomplicated GTCSs monitored in EMUs lead to leukocyte elevations within the normal range, [7] while GTCSs seen in the ED often lead to frank leukocytoses, particularly in cases of status epilepticus, [11] compromised breathing, [12] and postictal pulmonary edema. [13] Interestingly, in one recent study of aneurysmal subarachnoid hemorrhage, [14] both the troponin I and leukocyte count elevations were associated with the appearance of neurogenic pulmonary edema, which not only is frequently seen in SUDEP autopsies [15] but also appears to have contributed to this patient’s demise.…”

Hiding in plain sight? A review of post-convulsive leukocyte elevations

“…For instance, in patients admitted electively to an EMU, average PoCLEs occurred entirely within the normal leukocyte range (from 5,900 to 8,330 cells/mm 3 ; normal range 4,000–11,000 cells/mm 3 ) ( 65 ). Recently we estimated that 89.5% of 105 patients hospitalized with GCSs experienced PoCLEs either within or above the normal leukocyte range ( 68 ). Therefore, paraphrasing from an early publication ( 55 ), it is likely that GCSs in otherwise healthy patients invariably cause temporary elevations of the leukocyte count.…”

“…In a different line of investigation, Tiamkao and Sawanyawisuth studied predictors of death in 32 cases of generalized CSE treated with sodium valproate and concluded that, when found at presentation, post-convulsive leukocytosis was associated with death ( 74 ). Recently, one of these authors (JLV) and colleagues, found a significant correlation between the degree of PoCLEs and the presence of periconvulsive signs of respiratory distress ( 68 ). As that study also revealed a statistically significant correlation between post-convulsive leukocyte counts and ED triage heart rates, it was hypothesized that aside from inducing PoCLEs catecholamines might play a role in producing, or in exacerbating, periconvulsive respiratory symptoms.…”

Diagnostic and predictive value of white blood cell count, erythrocyte sedimentation rate, and coagulation tests in patients with blunt head trauma

“…[19][20][21] The normal WBC count is 1 to 4 WBC per microliter (LCM). 22 An increase in the number of WBC is called leukocytosis. 23 Leukocytosis is generally present in: infectious diseases, inflammatory diseases (such as rheumatoid arthritis and allergies), some neoplasms such as leukemia, severe mental or physical stress, and tissue damage (severe burns).…”