- Email: [email protected]
Cavernous sinus thrombosis: A rare complication of sinusitis
INTEI~qATMINALJOQNALOF
ELSEVIER
International Journal of Pediatric Otorhinolaryngology 39 (1997) 77-83
III
Case report
Cavernous sinus thrombosis: a rare complication of sinusitis A. Onur Odaba~l ~'*, Ay~e Akgfilb aState Hospital of Mu~,la, Department of Otolaryngology, Mu~,la, Turkey bState Hospital of Mu~,la, Department of Injectious Diseases, Mu~la, Turkey Received 30 August 1996: accepted 14 October 1996
Abstract
Intracranial complications of sinusitis are infrequent since the advent of antibiotics, and furthermore the prognosis is improved by medical therapy. We have seen a patient with an intracranial complication of sinus infection that had a history of frontal bone trauma five years ago. Then following an upper respiratory tract infection, headache, bilateral periorbital pain and swelling, spiking fever, neck stiffness, bilateral chemosis and ophthalmoplegy developed. Cavernous sinus thrombosis was diagnosed clinically and high doses of I.V. antibiotics were started promptly. The patient's condition improved in the first week of her admission. She was discharged three weeks later, without any surgical intervention. Two-year follow up showed no cranial nerve palsies or any neurologic deficiencies. A good result has been achieved by immediate medical measures. © 1997 Elsevier Science Ireland Ltd. All rights reserved
Keywords: Cavernous sinus thrombosis; Intracranial complication; Sinusitis
* Corresponding author. Present address: Adnan Menderes University, School of Medicine, Department of Otolaryngology, Aydin, Turkey 09100. Fax: + 90 256 2120146.
0165-5876/97/$17.00 © 1997 Elsevier Science Ireland Ltd. All rights reserved PI1 $01 65-5876(96)01 46 1-9
78
A.O. Odaba¢t, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77 83
I. Introduction
The total number of cases of sinus infections with intracranial complications has decreased since the advent of antibiotics. The cases of chronic sinusitis with infrequent bouts of acute infection are now the prime offenders. The most common predisposing factor to intracranial complication is altered sinus physiology due to chronic sinusitis. This may be the result of infection, drug abuse, chemical exposure or trauma. Frontal sinus is the most often involved with the intracranial complications following ethmoid, sphenoid and maxillary sinuses.
2. Case report
G.D., a 12 year old female, was admitted as an urgent case with frontal headache, bilateral orbital pain and periorbital swelling, vomiting and neck stiffness to the State Hospital of Mu~la in October 1993. She had a rapidly augmenting confusion. Her past medical history revealed a head trauma five years ago and she had been admitted to the neurosurgery department for observation. In the previous 5 years, she had been treated for several attacks of purulent rhinitis and sinusitis. Physical examination showed bilateral periorbital edema (more prominent on the right side), chemosis and significant swelling involving the right eye which was extending from forehead to right ear. High fever; (40°C) and confusion were present at the time of admission (Fig. 1). Bilateral, 10-12 hemorrhagic spots had been observed at the gluteal and abdominal region. Neck stiffness and positive Brudzinsky sign were present. ENT examination showed right sided muco-purulent
!ii~¸'¸i
!~!~lmmlllmP'
Fig. 1. Bilateral periorbital edema extendingfrom forehead to right cheek.
A.O. Odaba~,~, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77-83
79
Fig. 2. Waters view showing right frontal and ethmoid sinus opacification and right maxillary sinus mucosal hypertrophy.
nasal discharge, edematous nasal mucosa and bilateral inferior turbinate hypertrophy. Otoscopy was bilaterally normal. Complete blood count showed, PNL: 15100/ram3; Hb: 12.5 g/dl; platelets: 75000/mm 3. Sinus X-rays revealed right sided frontal and ethmoid sinus opacification (Fig. 2). Lumbar puncture performed on the same day, showed increased CSF pressure, elevated protein and low glucose levels. Cell count was 2300/mm 3 (PNL dominant). CSF culture was sterile. Intravenous penicillin (24 million units/day), chloramphenicol (2 g/day) and dexamethasone were started on the same day. On the second day of admission, spiking fever and right sided sixth cranial nerve palsy developed. Ophthalmology consultation revealed engorged retinal veins and papilloedema. Both globes appeared fixated in the primary position. Swelling over the roof of the nose and frontal region (Pott's puffy tumor) and hypoesthesia of the infraorbital region was noticed (Fig. 3). Pus was aspirated from beneath the skin of her swollen forehead but the culture was sterile. Two days later, her fever increased, confusion deepened and seizure activity was noticed at the right side of the face. The antibiotics were changed to I.V. Sulbactam and Cephaperazone (2 g/day). Two days later the patient's condition started to improve. Neck stiffness disappeared, she became conscious and fever was 37°C. She began to tolerate P.O. fluids. The patient was discharged 24 days later, with only right sided sixth cranial nerve palsy (Fig. 4). Two-year follow-up showed no neurologic deficit and no ophthalmologic pathologic findings (Fig. 5).
80
A.O. Odaba~l, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77 83
Fig. 3. Right chemosis, fixed globe and fixed pupil. 3. Discussion
Previous studies have shown that the incidence of frontal sinusitis has not declined since introduction of penicillin, however, the overall incidence of complicating intracranial infection has decreased [6]. Bluestone states that 10% of all patients hospitalized for treatment of frontal sinusitis still develop intracranial
Fig. 4. Right sided N. abducens paralysis and ptosis.
A.O. Odaba~;t, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77-83
81
Fig. 5. Two-year follow-up showed complete recovery.
complications. The possible intracranial complications from disease of nasal passages and sinuses are external and internal pachymeningitis, ieptomeningitis, extradural and subdural abscess, dural fistula, the various types of brain abscesses and septic thrombosis of cavernous or superior longitudinal sinuses. Infections from the nose and sinuses may invade the intracranial structures after trauma, through congenital dehiscence or non closure of fetal defects, by a direct pathway through the sinus wall, along the sheaths of the olfactory nerves, by way of communicating veins, by means of septic thrombi along the diploic veins with a retrograde thrombophlebitis or periphlebitis to the cavernous sinus, by way of the angular or ethmoidal veins to the cavernous sinus and by way of the orbit [5]. Adolescence is also associated with a peak in the vascularity of the diploic system and continued growth of the frontal sinus. These factors may increase the risk of suppurative extension of these infections [2]. In the case we presented, the frontal bone trauma and adolescence have been suggested as the etiologic factors for the extension of the infection to the intracranial structures. Cavernous sinus thrombosis, was first described by Bright in 1831 as a sequel of both epidural and subdural infections. This process is often a rapidly progressive one in which the sepsis reaches the cavernous sinus by direct extension of the infected thrombus or a shower of septic emboli [1]. Symptoms include orbital pain (V1) with venous congestion of the retina, lids and conjunctiva. The eyes are proptosed with exophthalmos. The patient has photophobia and involvement of II, III, IV, V cranial nerves. Fever spikes, chills and tachycardia may appear if
82
,4.0. Odaba~t, A. Akgiil / Int. J. Pediatr. Otorhinolarvngol. 39 (1997) 77-83
generalized septicemia is present. Seizure activity and/or hemiparesis may occur if wide spread cortical vein thrombosis or meningitis develops. Price et al. believed that unilateral ocular involvement in association with meningitis or an isolated contralateral palsy may represent an early cavernous sinus thrombosis. Ptosis, diplopia and photophobia have also been cited as premonitory symptoms of cavernous sinus thrombosis [4]. Diagnosis is primarily made on clinical evaluation. Lumbar puncture is usually sterile. The most frequently cultured organisms in all of the intracranial complications of frontal sinus origin are non beta hemolytic Streptococci, many of which are anaerobic or microaerophilic. Staphylococcus, pneumococcus and enterobacteriacae account for the remainder of the organisms found in these infections [6]. Negative cultures for aerobes and anaerobes may occur most likely because of empiric antibiotic therapy prior to surgical intervention. CT with contrast may show the source of infection and cavernous sinus involvement. Treatment should start with high dose antibiotics. I.V. high dose penicillin and chloramphenicol are the first choice of antibiotics. The discovery of pituitary inflammation at autopsy has suggested the use of steroids to control adrenal insufficiency and vascular collapse. Steroid assay during the course of the disease would seem to be indicated [3]. Use of anticoagulants for cavernous sinus thrombosis is still controversial. Some authors believe they will prevent the propagation of the clot. Others, including Yarington, think that the clot confines the bacterial spread via septic emboli. He reviewed 878 cases and came to the conclusion that it should not to be used [1,7]. On review of 874 reported cases of cavernous sinus thrombosis, Yarington calculated a mortality rate of 80%, and a morbidity rate of 75% among the survivors [7]. The most common sequelae are persistent cranial nerve palsies in 30% and blindness in 15% of the patients. Although surgery was not performed at the time of diagnosis and the patient was managed medically, her follow-up by the end of the second year did not show any cranial nerve deficiencies. It must be emphasized that treatment of the intracranial complications assumes priority over the underlying frontal sinus disease. If possible, however the sinus infection should be drained at the same time as the surgical treatment of the intracranial complication. In our case, the frontal sinus cleared by medical management alone. Frontal sinus infection extends to the intracranial space by septic retrograde thrombophlebitis. The high resolution CT scan with contrast is an effective method for diagnosis, but the condition may also be diagnosed by clinical evaluation and by means of direct sinus X-rays. We presented a case with frontal sinus infection that developed an intracranial complication, and improved with only medical management. Two year follow-up showed no cranial nerve palsy or any neurologic deficiency.
A.O. Odaba¢t, A. Akgiil lint. J. Pediatr. Otorhinolaryngol. 39 (1997) 77 83
83
References [1] Blitzer, A., Carmel, P. (1985) Intracranial complications of disease of the paranasal sinuses. In: Blitzer, A., Lawson, W., Friedman, W., (Eds.) Surgery of the Paranasal Sinuses. Philadelphia, W.B. Saunders, pp. 328-337. [2] Clayman, G., Adams, G., Paugh, D. et al. (1991) lntracranial complications of paranasal sinusitis: a combined institutional review. Laryngoscope, 101,234 239. [3] Fairbanks, D., Vanderveen, T., Bordlet, J. (1988) intracranial complication of sinusitis. In: English, G (Ed.) Otolarnygology, Vol. 2, Philadelphia, J.B. Lippincott, pp. 1 27. [4] Lawson, W. (1985) Orbital complications of the sinusitis. In: Blitzer, A., Lawson, W., Friedman, W. (Eds.) Surgery of Paranasal Sinuses, Philadelphia, W.B.Saunders, pp. 316-327. [5] Montgomery, W., Singer, M., Hamaker, R. (1985) Complications of sinus disease. In: Ballenger, J. (Ed.) Diseases of the Nose, Throat, Ear, Head and Neck, 13th edn, Philadelphia, Lea and Febiger, pp. 247 248. [6] Remmler, D. and Boles, R. (1980) Intracranial complications of frontal sinusitis. Laryngoscope, 90, 1814 1824. [7] Yarington, C. (1961) The prognosis and treatment of cavernous sinus thrombosis. Ann. Otol. Rhinol. Laryngol. 70, 263.
ELSEVIER
International Journal of Pediatric Otorhinolaryngology 39 (1997) 77-83
III
Case report
Cavernous sinus thrombosis: a rare complication of sinusitis A. Onur Odaba~l ~'*, Ay~e Akgfilb aState Hospital of Mu~,la, Department of Otolaryngology, Mu~,la, Turkey bState Hospital of Mu~,la, Department of Injectious Diseases, Mu~la, Turkey Received 30 August 1996: accepted 14 October 1996
Abstract
Intracranial complications of sinusitis are infrequent since the advent of antibiotics, and furthermore the prognosis is improved by medical therapy. We have seen a patient with an intracranial complication of sinus infection that had a history of frontal bone trauma five years ago. Then following an upper respiratory tract infection, headache, bilateral periorbital pain and swelling, spiking fever, neck stiffness, bilateral chemosis and ophthalmoplegy developed. Cavernous sinus thrombosis was diagnosed clinically and high doses of I.V. antibiotics were started promptly. The patient's condition improved in the first week of her admission. She was discharged three weeks later, without any surgical intervention. Two-year follow up showed no cranial nerve palsies or any neurologic deficiencies. A good result has been achieved by immediate medical measures. © 1997 Elsevier Science Ireland Ltd. All rights reserved
Keywords: Cavernous sinus thrombosis; Intracranial complication; Sinusitis
* Corresponding author. Present address: Adnan Menderes University, School of Medicine, Department of Otolaryngology, Aydin, Turkey 09100. Fax: + 90 256 2120146.
0165-5876/97/$17.00 © 1997 Elsevier Science Ireland Ltd. All rights reserved PI1 $01 65-5876(96)01 46 1-9
78
A.O. Odaba¢t, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77 83
I. Introduction
The total number of cases of sinus infections with intracranial complications has decreased since the advent of antibiotics. The cases of chronic sinusitis with infrequent bouts of acute infection are now the prime offenders. The most common predisposing factor to intracranial complication is altered sinus physiology due to chronic sinusitis. This may be the result of infection, drug abuse, chemical exposure or trauma. Frontal sinus is the most often involved with the intracranial complications following ethmoid, sphenoid and maxillary sinuses.
2. Case report
G.D., a 12 year old female, was admitted as an urgent case with frontal headache, bilateral orbital pain and periorbital swelling, vomiting and neck stiffness to the State Hospital of Mu~la in October 1993. She had a rapidly augmenting confusion. Her past medical history revealed a head trauma five years ago and she had been admitted to the neurosurgery department for observation. In the previous 5 years, she had been treated for several attacks of purulent rhinitis and sinusitis. Physical examination showed bilateral periorbital edema (more prominent on the right side), chemosis and significant swelling involving the right eye which was extending from forehead to right ear. High fever; (40°C) and confusion were present at the time of admission (Fig. 1). Bilateral, 10-12 hemorrhagic spots had been observed at the gluteal and abdominal region. Neck stiffness and positive Brudzinsky sign were present. ENT examination showed right sided muco-purulent
!ii~¸'¸i
!~!~lmmlllmP'
Fig. 1. Bilateral periorbital edema extendingfrom forehead to right cheek.
A.O. Odaba~,~, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77-83
79
Fig. 2. Waters view showing right frontal and ethmoid sinus opacification and right maxillary sinus mucosal hypertrophy.
nasal discharge, edematous nasal mucosa and bilateral inferior turbinate hypertrophy. Otoscopy was bilaterally normal. Complete blood count showed, PNL: 15100/ram3; Hb: 12.5 g/dl; platelets: 75000/mm 3. Sinus X-rays revealed right sided frontal and ethmoid sinus opacification (Fig. 2). Lumbar puncture performed on the same day, showed increased CSF pressure, elevated protein and low glucose levels. Cell count was 2300/mm 3 (PNL dominant). CSF culture was sterile. Intravenous penicillin (24 million units/day), chloramphenicol (2 g/day) and dexamethasone were started on the same day. On the second day of admission, spiking fever and right sided sixth cranial nerve palsy developed. Ophthalmology consultation revealed engorged retinal veins and papilloedema. Both globes appeared fixated in the primary position. Swelling over the roof of the nose and frontal region (Pott's puffy tumor) and hypoesthesia of the infraorbital region was noticed (Fig. 3). Pus was aspirated from beneath the skin of her swollen forehead but the culture was sterile. Two days later, her fever increased, confusion deepened and seizure activity was noticed at the right side of the face. The antibiotics were changed to I.V. Sulbactam and Cephaperazone (2 g/day). Two days later the patient's condition started to improve. Neck stiffness disappeared, she became conscious and fever was 37°C. She began to tolerate P.O. fluids. The patient was discharged 24 days later, with only right sided sixth cranial nerve palsy (Fig. 4). Two-year follow-up showed no neurologic deficit and no ophthalmologic pathologic findings (Fig. 5).
80
A.O. Odaba~l, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77 83
Fig. 3. Right chemosis, fixed globe and fixed pupil. 3. Discussion
Previous studies have shown that the incidence of frontal sinusitis has not declined since introduction of penicillin, however, the overall incidence of complicating intracranial infection has decreased [6]. Bluestone states that 10% of all patients hospitalized for treatment of frontal sinusitis still develop intracranial
Fig. 4. Right sided N. abducens paralysis and ptosis.
A.O. Odaba~;t, A. Akgiil / Int. J. Pediatr. Otorhinolaryngol. 39 (1997) 77-83
81
Fig. 5. Two-year follow-up showed complete recovery.
complications. The possible intracranial complications from disease of nasal passages and sinuses are external and internal pachymeningitis, ieptomeningitis, extradural and subdural abscess, dural fistula, the various types of brain abscesses and septic thrombosis of cavernous or superior longitudinal sinuses. Infections from the nose and sinuses may invade the intracranial structures after trauma, through congenital dehiscence or non closure of fetal defects, by a direct pathway through the sinus wall, along the sheaths of the olfactory nerves, by way of communicating veins, by means of septic thrombi along the diploic veins with a retrograde thrombophlebitis or periphlebitis to the cavernous sinus, by way of the angular or ethmoidal veins to the cavernous sinus and by way of the orbit [5]. Adolescence is also associated with a peak in the vascularity of the diploic system and continued growth of the frontal sinus. These factors may increase the risk of suppurative extension of these infections [2]. In the case we presented, the frontal bone trauma and adolescence have been suggested as the etiologic factors for the extension of the infection to the intracranial structures. Cavernous sinus thrombosis, was first described by Bright in 1831 as a sequel of both epidural and subdural infections. This process is often a rapidly progressive one in which the sepsis reaches the cavernous sinus by direct extension of the infected thrombus or a shower of septic emboli [1]. Symptoms include orbital pain (V1) with venous congestion of the retina, lids and conjunctiva. The eyes are proptosed with exophthalmos. The patient has photophobia and involvement of II, III, IV, V cranial nerves. Fever spikes, chills and tachycardia may appear if
82
,4.0. Odaba~t, A. Akgiil / Int. J. Pediatr. Otorhinolarvngol. 39 (1997) 77-83
generalized septicemia is present. Seizure activity and/or hemiparesis may occur if wide spread cortical vein thrombosis or meningitis develops. Price et al. believed that unilateral ocular involvement in association with meningitis or an isolated contralateral palsy may represent an early cavernous sinus thrombosis. Ptosis, diplopia and photophobia have also been cited as premonitory symptoms of cavernous sinus thrombosis [4]. Diagnosis is primarily made on clinical evaluation. Lumbar puncture is usually sterile. The most frequently cultured organisms in all of the intracranial complications of frontal sinus origin are non beta hemolytic Streptococci, many of which are anaerobic or microaerophilic. Staphylococcus, pneumococcus and enterobacteriacae account for the remainder of the organisms found in these infections [6]. Negative cultures for aerobes and anaerobes may occur most likely because of empiric antibiotic therapy prior to surgical intervention. CT with contrast may show the source of infection and cavernous sinus involvement. Treatment should start with high dose antibiotics. I.V. high dose penicillin and chloramphenicol are the first choice of antibiotics. The discovery of pituitary inflammation at autopsy has suggested the use of steroids to control adrenal insufficiency and vascular collapse. Steroid assay during the course of the disease would seem to be indicated [3]. Use of anticoagulants for cavernous sinus thrombosis is still controversial. Some authors believe they will prevent the propagation of the clot. Others, including Yarington, think that the clot confines the bacterial spread via septic emboli. He reviewed 878 cases and came to the conclusion that it should not to be used [1,7]. On review of 874 reported cases of cavernous sinus thrombosis, Yarington calculated a mortality rate of 80%, and a morbidity rate of 75% among the survivors [7]. The most common sequelae are persistent cranial nerve palsies in 30% and blindness in 15% of the patients. Although surgery was not performed at the time of diagnosis and the patient was managed medically, her follow-up by the end of the second year did not show any cranial nerve deficiencies. It must be emphasized that treatment of the intracranial complications assumes priority over the underlying frontal sinus disease. If possible, however the sinus infection should be drained at the same time as the surgical treatment of the intracranial complication. In our case, the frontal sinus cleared by medical management alone. Frontal sinus infection extends to the intracranial space by septic retrograde thrombophlebitis. The high resolution CT scan with contrast is an effective method for diagnosis, but the condition may also be diagnosed by clinical evaluation and by means of direct sinus X-rays. We presented a case with frontal sinus infection that developed an intracranial complication, and improved with only medical management. Two year follow-up showed no cranial nerve palsy or any neurologic deficiency.
A.O. Odaba¢t, A. Akgiil lint. J. Pediatr. Otorhinolaryngol. 39 (1997) 77 83
83
References [1] Blitzer, A., Carmel, P. (1985) Intracranial complications of disease of the paranasal sinuses. In: Blitzer, A., Lawson, W., Friedman, W., (Eds.) Surgery of the Paranasal Sinuses. Philadelphia, W.B. Saunders, pp. 328-337. [2] Clayman, G., Adams, G., Paugh, D. et al. (1991) lntracranial complications of paranasal sinusitis: a combined institutional review. Laryngoscope, 101,234 239. [3] Fairbanks, D., Vanderveen, T., Bordlet, J. (1988) intracranial complication of sinusitis. In: English, G (Ed.) Otolarnygology, Vol. 2, Philadelphia, J.B. Lippincott, pp. 1 27. [4] Lawson, W. (1985) Orbital complications of the sinusitis. In: Blitzer, A., Lawson, W., Friedman, W. (Eds.) Surgery of Paranasal Sinuses, Philadelphia, W.B.Saunders, pp. 316-327. [5] Montgomery, W., Singer, M., Hamaker, R. (1985) Complications of sinus disease. In: Ballenger, J. (Ed.) Diseases of the Nose, Throat, Ear, Head and Neck, 13th edn, Philadelphia, Lea and Febiger, pp. 247 248. [6] Remmler, D. and Boles, R. (1980) Intracranial complications of frontal sinusitis. Laryngoscope, 90, 1814 1824. [7] Yarington, C. (1961) The prognosis and treatment of cavernous sinus thrombosis. Ann. Otol. Rhinol. Laryngol. 70, 263.