Death From a Stuffy Nose

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Complicated sinusitis can sometimes have devastating effects.

Background

Sinusitis is inflammation of the paranasal sinus mucous membranes. It is characterized by drainage, congestion, anosmia, cough, facial tenderness or headache. Involvement of all four sinuses; maxillary, sphenoid, frontal and ethmoid is called pansinusitis. [1] Complications of sinusitis are rare, occurring in approximately 15% of complicated sinusitis. [2]


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Acute cerebral infarct - fig 1

Initial CT head without contrast obtained at outside hospital when patient first presented with headache and sinus pain showing sinusitis without cerebral infarction.

Spread of the infection from the sinuses can occur including to the bone, central nervous system and surrounding tissue. [1,2] Such complications include septal and pre-septal cellulitis, intracranial abscess, sub-periosteal abscess, osteomyelitis, cavernous sinus thrombosis and meningitis. [3] Meningitis from any cause has mortality between 10% to 30%. [4]

Traditional causes of cerebral ischemia include ischemic and hemorrhagic causes. Suggested pathophysiology for infectious cause of cerebral infarction involves local inflammation of blood vessels and cerebritis. [5] Acute cerebral infarct from severe sinus infection was discussed most comprehensively in a retrospective study of 12 patients with purulent complications of frontal sinusitis by Betz et al. [2]

Case Presentation


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A 54-year-old Caucasian male with a past medical history of hypertension and high cholesterol presented as a transfer to our tertiary intensive care unit with an admitting diagnosis of pansinusitis and left frontal parietal cerebral infarct after being seen at an remote emergency room. He was transferred for treatment of ischemic complications of pansinusitis. On physical exam, vital signs were remarkable for fever of 103.8F, blood pressure 133/67, heart rate 77, respiratory rate 30 breaths per minute, oxygen saturation 99% room air.

Initial labs showed WBC of 17,900 with 82% neutrophils and 4 bands (Hemoglobin12.7, platelets 320), CMP was only remarkable for fasting blood glucose of 160. Initial lactic acid was 10. The patient had gaze preference to the left, visual reaction to confrontation was intact, pupils were equally reactive.

He did not respond with grimace on palpation of his face and he was aphasic. Patient had right sided hemiplegia, clonus of the right lower extremity and bilateral lower extremity hyperreflexia. Glascow Coma Scale was approximately 10 (Eyes=4, Verbal=2, Motor=4). His respirations were adequate with regard to rate and depth, but patient needed to be intubated to protect his airway from secretions.

Acute cerebral infarct - fig 2

Initial CT head without contrast obtained at outside hospital when patient first presented with headache and sinus pain showing sinusitis without cerebral infarction.

MRI with contrast of the brain showed large acute ischemic infarction on the inferior anterior left frontal lobe with positive restricted diffusion extending to the anterior left temporal lobe, basal ganglia and left internal capsule. There was no enhancement identified. There was complete opacification of the sinuses suggesting severe pan-sinusitis. No abscess or empyemas were seen.


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CT angiography did not show any inflammation or infection of the major cerebral vessels although microvascular invasion could not be completely ruled out. No stenosis or occlusion of vessels in the area affected. There was no osteomyelitis to suggest direct spread through bone surrounding sinus. Venous sinuses were also patent without thrombosis.  Other labs obtained suggested undiagnosed diabetes with fasting blood sugar of 160 and Hemoglobin A1C of 6.8%.

Broad spectrum intravenous antibiotics including antifungal therapy were started based on infectious disease physician recommendation which included vancomycin, cefepime, flagyl and amphotericin B. Cerebral spinal fluid analysis (CSF) on day two was consistent with bacterial meningitis. Endoscopic surgery through the nares where incision and drainage were completed by an ear nose throat physician showed nasal polyposis as well as purulent drainage from frontal, sphenoid, bilateral maxillary and ethmoid sinuses.

Subsequently, positive Streptococcus pneumonia blood cultures were reported from the transferring hospital. Our patient subsequently deteriorated and was minimally responsive off sedation. His family elected to pursue comfort care after one week of treatment and the patient died.

Conclusions

Our patient had meningitis without abscess from pansinusitis that led to cerebral infarction presumably from localized inflammation of cerebral vessels and cerebritis. The identified bacteria causing the infection was confirmed to be a Strep. pneumonia infection identified by CSF and blood cultures.

An observational cross sectional study found that occurrence rate of cerebral infarction in patients suffering from meningitis with concurrent diagnosis of sinusitis or otitis was found to be 35% compared with 22%.[5]

Acute cerebral infarct - fig 3

MRI showing acute fronto-parietal infarct day.

Risk factors for development of cerebral infarction during meningitis were age, streptococcus pneumonia positive CSF cultures, lower CSF white blood cell count, higher erythrocyte sedimentation rate, and presence of predisposing conditions such as otitis, sinusitis and immunocompromised conditions. Patients with cerebral infarctions were also more likely to present with fever, nuchal rigidity and altered level of consciousness.[5]  Our patient had fever and confusion when he first presented to a health care facility.

Autopsy findings of patients who have died from cerebral infarctions associated with meningitis have suggested the mechanism of death is cerebral vasculitis, inflammatory infiltration of cerebral arteries and veins, and segmental narrowing leading to ischemic infarct.[5] However, as in our case, cerebral infarctions have occurred in patients with normal angiographic studies. [4,5]  Other proposed mechanisms include vasospasm and activation of coagulation pathway.[5]

Up to 54% of infarctions will not be present on admission in patients with meningitis.[5]  This case highlights the need for more aggressive work up when patients present with severe sinusitis symptoms when they present to the emergency room.

Additionally, patients with history of sinusitis have a baseline increased risk of stroke through traditional mechanisms of thrombosis and hemorrhage. A prospective cohort study in Taiwan by Wu et al, which followed patients with outpatient diagnosis of acute or chronic sinusitis for development of stroke over three years found that sinusitis is a risk factor for stroke.[7] Acute sinusitis had a higher hazard ratio compared to chronic sinusitis.

Acute cerebral infarct -fig 4

MRI showing acute fronto-parietal infarct day.

CT of the sinuses is the most specific and sensitive imaging method for sinusitis; however, this should be reserved for cases not responsive to traditional treatment. Contrast should be used for patients with focal deficits. MRI should also be used if there are neurological symptoms.

Treatment is aimed at decongestants and pain control as viral upper respiratory infections are thought to be the precipitating cause. Beyond day seven of symptoms, begin treatment with antibiotics aimed at Strep pneumonia and Haemophilus, which are implicated in a majority of cases. Patients with complicated sinusitis should be admitted and treated with broad spectrum antibiotics.

Reference List

  1. Hwang, PH, Patel, Z. “Acute Sinusitis and Rhinosinusitis in Adults: Clinical Manifestations and Diagnosis.” 22 Jan. 16. Accessed 13 Feb 2016.
  2. Betz C, Issing W, Matschke J, Kremer A, Uhl E, Leunig A. Complications of acute frontal sinusitis: a retrospective study. European Archives Of Oto-Rhino-Laryngology: Official Journal Of The European Federation Of Oto-Rhino-Laryngological Societies (EUFOS): Affiliated With The German Society For Oto-Rhino-Laryngology – Head And Neck Surgery [serial online]. January 2008;265(1):63-72. Available from: MEDLINE Complete, Ipswich, MA. Accessed February 13, 2016.
  3. Hamilos, Daniel L. “Chronic Rhinosinusitis: Management.” Uptodate. 22 Oct. 2015. Web. 13 Feb. 2016.
  4. Pfister HW, Borasio GD, Dirnagl U, Bauer M, Einhaupl KM. Cerebrovascular complications of bacterial meningitis in adults. Neurology. 1992;42:1497–504.
  5. Schut ES, Lucas MJ, Brouwer MC, Vergouwen MD, van der Ende A, Van de Beek D.. Cerebral infarction in adults with bacterial meningitis. Neurocrit Care 2012;16:421–427
  6. Wu C, Chao P, Hao W, Liou T, Lin H. Risk of stroke among patients with rhinosinusitis: a population-based study in Taiwan. American Journal Of Rhinology & Allergy [serial online]. July 2012;26(4):278-282. Available from: MEDLINE Complete, Ipswich, MA. Accessed January 31, 2016.
  7. Jauch EC, Barbabella SP, Fernandez FJ, Knoop KJ. Chapter 5. Ear, Nose, and Throat Conditions. In: Knoop KJ, Stack LB, Storrow AB, Thurman R. eds. The Atlas of Emergency Medicine, 3e. New York, NY: McGraw-Hill; 2010. http://accessmedicine.mhmedical.com.ezproxy.med.wmich.edu/content.aspx?bookid=351&Sectionid=39619704. Accessed January 30, 2016.

ABOUT THE AUTHOR

Dr. Crafton is an Emergency Medicine Physician at Southern Arizona VA Healthcare System. She also serves as a preceptor for emergency medicine residents from University of Arizona Emergency Medicine residency program.

1 Comment

  1. peter j gruber on

    From an EM point of view, it would be interesting to know how this patient initially presented to the hospital. Was the pt already very sick when he presented? Had he been seen previously regarding this? We see many pts who we suspect have sinusitis but we generally dont image them if they arent toxic appearing, showing signs of CNS infection or immunocompromised. We give these patients discharge instructions regarding what to come back for and with whom to follow up. The challenge as with all of medicine is to figure out early on
    which patient is at risk of developing worsening complications of their medical problem

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