Indian Journal of Dental Research

CASE REPORT
Year
: 2013  |  Volume : 24  |  Issue : 6  |  Page : 759--761

Postcraniofacial trauma multidrug resistant Acinetobacter Baumannii infection treated with intravenous colistin: A rare complication


Sanjay Rastogi1, Anurag Gupta2, Raja S Narne3, Mahendra P Reddy1, Mansi Bansal4, Sanjeev Kumar1,  
1 Department of Oral and Maxillofacial Surgery and Oral Implantology, ITS Dental College, Murad Nagar, India
2 Departments of Oral and Maxillofacial Surgery, Shree Bankey Bihari Dental College and Research Center, Ghaziabad, India
3 Sree Sai Dental College and Research Institute, Sreekakulam, Andhra Pradesh, India
4 Department of Periodontology, IDST, Kadrabad, Modinagar, India

Correspondence Address:
Sanjay Rastogi
Department of Oral and Maxillofacial Surgery and Oral Implantology, ITS Dental College, Murad Nagar
India

Abstract

Nosocomial meningitis is a rare complication of combined craniofacial and neurosurgical procedures. The increase in meningitis caused by multidrug-resistant (MDR) Acinetobacter baumannii has resulted in a significant reduction in available treatment options. We report a case of 52-year-old man who sustained a complex craniofacial trauma, who developed nosocomial MDR infection caused by A. baumannii in the wound. Patient was at significant risk of developing meningitis but, he was successfully treated with intravenous colistin. To conclude, patients with complex maxillofacial trauma are at high risk of MDR A. baumannii meningitis, especially in craniofacial intensive care units, and adequate infection control measures with proper institution of antibiotics, should be used to reduce the risk of this infection



How to cite this article:
Rastogi S, Gupta A, Narne RS, Reddy MP, Bansal M, Kumar S. Postcraniofacial trauma multidrug resistant Acinetobacter Baumannii infection treated with intravenous colistin: A rare complication.Indian J Dent Res 2013;24:759-761


How to cite this URL:
Rastogi S, Gupta A, Narne RS, Reddy MP, Bansal M, Kumar S. Postcraniofacial trauma multidrug resistant Acinetobacter Baumannii infection treated with intravenous colistin: A rare complication. Indian J Dent Res [serial online] 2013 [cited 2019 Nov 21 ];24:759-761
Available from: http://www.ijdr.in/text.asp?2013/24/6/759/127629


Full Text

Acinetobacter baumannii is a nosocomial pathogen of increasing importance. [1] Outbreaks of infection with the organism have been noted in every inhabited continent in the past decade, with nosocomial pneumonia being the most common clinical manifestation. Substantial concern has been the increasing prevalence of multidrug resistance in hospital isolates of A. baumannii during the past decade. The organism can possess an impressive armamentarium of resistance mechanisms-the end result being resistance to all, or almost all, commercially available antibiotics.

Craniofacial trauma and postneurosurgical patients have a high risk of developing nosocomial meningitis, with potentially lethal consequences. The widespread use of antibiotics may have altered the epidemiology of postneurosurgical meningitis in recent years. [2] During the past three decades, A. baumannii has emerged as an infectious agent of importance in hospitals worldwide, due to its ability to tolerate desiccation and to accumulate diverse mechanisms of resistance. We report the case of a craniomaxillofacial trauma patient who was at a risk to develop meningitis due to multidrug-resistant (MDR) A. baumannii that was cured by intravenous colistin.

Two forms of colistin are available commercially: CMS (also called sodium colistin methanesulphonate, colistin methanesulfonate, colistin sulfomethate, or colistimethate), which is used for parenteral and inhalation therapy, and colistin sulfate, which is used orally and for topical use. Great care is needed to avoid confusion between colistin (base) and CMS; it is essential not to use the terms interchangeably. It has been demonstrated recently that CMS is a prodrug of colistin. [2]

We report the case of a craniomaxillofacial trauma patient who was at a risk to develop meningitis due to MDR A. baumannii that was cured by intravenous colistin.

 Case Report



A 52-years-old male patient was admitted to our maxillofacial surgery unit with sustained craniomaxillofacial trauma. On initial examination, his GCS was 8/15 with left blow-out fracture and skin loss on the left temporal region [Figure 1]. There was C4 and C5 subluxation of the C-spine. CT scan reveals complete left blow-out fracture with medial canthal ligament detachment but, nasal complex was intact with no sign and symptoms of CSF rhinorrhoea. Subsequently, his GCS was improved to 14/15. Perioperative, antibiotic chemoprophylaxis with cefazolin was started, and considering the patient's condition, it was prolonged. On the fifth day after postadmission the patient presented with remittent fever (peak 38.8 o C). Blood investigations except white blood cells were within normal limits. Blood culture was done and culture was taken from the wound site on the left temporal region. Blood culture was negative but, from the wound it was positive for A. baumanniii which was MDR but sensitive to colistin. In lieu to prevent post-traumatic meningitis and further wound infection colistin was started intravenously 2.5 mg/kg/day in daily divided doses for 10 days. After this period of time, a routine culture was obtained and patient was free of A. Baumannii infection and subsequently, skin grafting was done along with open reduction and fixation of left blowout fracture.{Figure 1}

 Discussion



Acinetobacter spp is a Gram-negative coccobacillus that, during the past three decades, has emerged from an organism of questionable pathogenicity to an infectious agent of importance in hospitals worldwide. [3] The organism's ability to tolerate desiccation and to accumulate diverse mechanisms of resistance favor its long-term persistence in ICUs, where skin carriage may persist for weeks and months and the presence of Acinetobacter nosocomially in the hospital may be responsible for patient-to-patient spread. Environmental contamination and contamination of medical equipment may also play an important role in the transmission of A. baumannii in healthcare institutions. [4] In hospitalized patients it is also a common colonizer of the respiratory tract and skin, particularly in the intensive care unit setting. Bacterial meningitis caused by A. baumannii constitutes around 10% of Gram-negative and 4% of nosocomial meningitis. [5] The mortality rate of patients with neurosurgery-related Gram negative meningitis is about 33%. [6]

Acinetobacter meningitis typically occurs following neurosurgery and craniomaxillofacial trauma. Patients at risk for postcraniofacial trauma bacterial meningitis include those with cerebrospinal leakage, concomitant incision infection, prolonged duration of surgery, surgery that enters a sinus, increased severity of illness, prolonged external ventricular drainage, and need for repeat surgery. [7]

Fever and change in the conscious state is a typical sign of Acinetobacter meningitis. Meningeal signs, focal neurological signs, and seizure are found in a minority of patients. Increased CSF white blood cell counts (ranging from 100 to several thousand cells per μL) are typical, with higher counts presumably found in those with delays in clinical suspicion of infection. However, cases of true infection that has no CSF white blood cells have been reported. Typically, 75-100% of the white blood cells are polymorphonuclear cells. CSF protein is almost always raised, most typically being between 150 mg/L and 200 mg/L. CSF glucose may be normal or depressed but, in our case CSF culture was not taken.

The polymyxins exert their bactericidal activity by binding to the bacterial cell membrane and disrupting its permeability, which results in leakage of intracellular components. They also have the antiendotoxin activity.

These agents are rapidly bactericidal against many gram-negative bacteria. The polymyxin antimicrobials are poorly absorbed from the gastrointestinal tract. Colistin concentrates in the liver, kidney, muscle, heart, and lungs but does not consistently cross the blood-brain barrier in noninflamed meninges. The poor dialyzability of the polymyxins may be caused by their large molecular size and not their plasma or tissue-binding ability. Polymyxins are excreted primarily by the kidneys. Pharmacokinetic studies in the 1960s demonstrated that the serum half-life of these drugs increases from 6 h or less in individuals with normal renal function to 48 h or more in anuric patients. [8]

Owen and colleagues, [9] examined recently the in-vitro pharmacodynamics of colistin against A. baumannii clinical isolates. They found that colistin showed rapid killing in a concentration-dependent manner. Colistin exhibited modest postantibiotic effect, however. Their results suggest that monotherapy with CMS, the parenteral form of colistin, and long dosage intervals (e.g. 24 h) may be problematic for treatment of infections caused by colistin-heteroresistant A. baumannii, although these findings should be supplemented by clinical studies.

Colistin has good activity against Acinetobacter spp (MIC90% 2 mg/L), K pneumoniae (MIC90% 1 mg/L), E coli (MIC90% 2 mg/L), P aeruginosa (MIC90% 4 mg/L), and Enterobacter spp (MIC50% 1 mg/L).

Colistin dosing has ranged from 2.5 to 5.0 mg/kg/d in patients with normal renal function and is usually given two to four times a day. In the United Kingdom, for adult patients and children older than 12 years who have normal renal function and body weight more than 60 kg, a dosing regimen of 240 to 480 mg (3-6 million IU) of CMS per day in three divided doses is recommended. In patients who have normal renal function and body weight 60 kg or less, 4 to 6 mg/kg (50,000-75,000 IU/kg) of CMS per day divided in three doses is recommended. It is remarkable that there is a substantial difference in the recommended doses of the European and US products. The recommended upper limit dosage for a 60-kg patient with normal renal function is 480 mg of CMS per day for the European product and approximately 800 mg of CMS per day for the US product. [10] Several clinical studies from Europe reported that in critically ill adult patients with normal renal function and body weight more than 60 kg, CMS was administered intravenously in a dose of 9 million IU divided into three equal doses.

 Conclusion



Unfortunately, Acinetobacter meningitis is becoming an increasingly common clinical entity. More likely than not, the organism is multidrug resistant when it is encountered in intensive care units or craniomaxillofacial wards. Since colonization of respiratory secretions, urine, or wounds often precedes nosocomial Acinetobacter meningitis cases, infection control measures, particularly in ICUs, should be vigorously enforced to prevent person-to-person spread of Acinetobacter from colonized patients via healthcare personnel and fomites.

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