Year : 2010 | Volume
: 21 | Issue : 4 | Page : 715--719
H1N1 in dialysis units: Prevention and management
Ayman Karkar, Mohammed Abdelrahman, Manzur R Jasim, Wafa AlOyouni
Kanoo Kidney Centre, Department of Nephrology, Dammam Medical Complex, Dammam, Saudi Arabia
Department of Nephrology, Kanoo Kidney Centre, P.O. Box 11825, Dammam 31463
Dialysis patients are at increased risk of contracting influenza A H1N1 and developing serious illness. Increasing the awareness of dialysis patients and continuous education and training of medical staff on early recognition and management of influenza A H1N1 can help in saving the life of patients. Antiviral drugs and influenza vaccines are effective in providing adequate immunity in dialysis patients with strict implementation of infection control policies and procedures can help in preventing and controlling the dissemination of influenza A H1N1 in dialysis units. We report a case of a patient who presented with HINI influenza and developed acute kidney injury during his hospitalization and his course with disease.
|How to cite this article:|
Karkar A, Abdelrahman M, Jasim MR, AlOyouni W. H1N1 in dialysis units: Prevention and management.Saudi J Kidney Dis Transpl 2010;21:715-719
|How to cite this URL:|
Karkar A, Abdelrahman M, Jasim MR, AlOyouni W. H1N1 in dialysis units: Prevention and management. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2020 Nov 24 ];21:715-719
Available from: https://www.sjkdt.org/text.asp?2010/21/4/715/64657
Following the recent world threat of avian influenza that has been originated in Asia, a new epidemic of acute respiratory infections caused by influenza A (H1N1) virus emerged in Mexico in April 2009 and soon spread to the United States and the rest of the world. , Influenza A virus strains are assigned an H (or hemagglutinin) number and an N (or neuraminidase) number based on which forms of these two proteins the strain contains on its surface.  The structure of these proteins differs from strain to strain due to rapid genetic mutation in the viral genome.  The hemagglutinin gene of this 2009 pandemic H1N1 virus (2009 H1N1) belongs to the classical swine lineage, which was first introduced into swine populations around 1918. ,,
H1N1 has a unique combination of genes from different swine lineages that has not been identified previously in either swine or human populations, , and it is antigenically and genetically distinct from hemagglutinins of contemporary human seasonal influenza H1N1 virus. ,,,
The clinical presentation is variable and nonspecific, and ranges from self-limited febrile illness to sever pneumonia. Emergency warning signs that need urgent medical attention include severe or persistent vomiting, shortness of breath, pain or pressure in the chest or abdomen, sudden dizziness and confusion.  Diagnosis of the 2009 H1N1 virus is confirmed by a qualitative positive RT-PCR test from a properly obtained nasal and/or throat swabs. ,
The risk factors of severe H1N1 illness include young age, obesity, pregnancy and chronic medical conditions such as cardiovascular diseases, diabetes mellitus, bronchial asthma and chronic renal failure. However, immune deficient patients are also at increased risk of developing severe or life threatening disease. 
A 43-year-old male technician who lived with 40 other residents in a camp, presented to the emergency room on 06 August 2009 with a 5-day history of progressive rise in temperature, cough, runny nose, sore throat, headache, body aches, fatigue, shortness of breath and chest pain, which increases on coughing or taking deep breath. Few inhabitants of his camp had mild cough but no fever. The patient and his camp mates had no history of recent travel abroad, and had no past history of any major medical illness or drug intake.
On physical examination the patient's temperature was 39.5C, regular pulse rate 90 beats/ min, blood pressure 133/75 mmHg, respiratory rate 30/min, O 2 saturation 95% and body weight 85 kg. His throat examination showed congestion and there were bilateral crackles on chest auscultation, but no other positive findings were detected on the rest of physical examination.
The throat and nasopharyngeal swabs were obtained on admission and tested positive for influenza-A H1N1 (2009 H1N1) by molecular pathology that included RNA extraction and cDNA extraction for real time-polymerase chain reaction. Chest X-ray revealed bilateral pulmonary infiltration. A diagnosis of community acquired pneumonia due to H1N1 virus was entertained, and the patient was admitted in an isolated room and started on oseltamivir 75 mg twice daily and broad spectrum antibiotics. However, the patient's symptoms progressed rapidly and within few hours of admission he developed respiratory failure, which necessitate intubation and assisted ventilation using high flow oxygen in an isolated negatively pressured room in the intensive care unit (ICU).
Three days following admission the patient developed generalized convulsions, where brain CT scan revealed hypodense areas in bilateral basal ganglia. His convulsions were controlled with phenytoin and diazepam. However, the patient developed severe nosocomial sepsis due to Acinetobacter central line infection. The culture and sensitivity of nasal swabs and chest secretions revealed multi-drug resistant Acinetobacter baumanii sensitive to tigecycline and colistin. He was covered with multiple antimicrobial agents including vancomycin, colistin, imipenem and tazocine according to clinical response and blood/secretions culture and sensitivity reports. Urine culture and sensitivity revealed Candida albicans urinary tract infection which was sensitive to voriconazole.
Subsequently, the patient developed acute kidney injury, which was evident by oligo-anuria and rapid rise in serum urea (55, 153 and 227 mg/dL) and creatinine (1.3, 3.5 and 7.5 mg/dL), hyperkalemia (K + 6.2 mmol/dL) with severe metabolic acidosis (pH 7.2 and HCO 3 17.7). The associated hypotension (BP ≤ 90/50 mmHg) and hemodynamic instability of the patient necessitated initiation of continuous renal replacement therapy (CRRT) on the 3rd day after admission, which was continued for 180 hours over the subsequent 18 days till the hemodynamic status of the patient was stabilized without the need for inotropic support. The oseltamivir dose was adjusted accordingly and continued for five days. Repeated throat and nasal swabs performed on the 18 th day of admission were negative for H1N1. After 3 weeks of stay in the hospital, the patient showed a significant clinical recovery of pneumonia, and it was possible to wean him off the ventilator. His renal function showed a significant improvement with progressive increase in urine output (initially up to 480 mL/24hr, 1100, 1600, 1900 and 2600 mL/24hr) and stabilization of serum urea (84 mg/dL) and creatinine (2.2 mg/ dL). During the following few days the patient made complete recovery of renal function, and he was shifted to the medical ward and subsequently discharged after one month of hospitalization.
During the patient's admission to the hospital, all the infection control policies and procedures were strictly applied, and all precautions were taken to avoid transmission of H1N1 virus.
Despite the early presentation with the expected common mild signs and symptoms of viral influenza, this reported case demonstrates the clinical evolvement into the possible worse scenario of the H1N1 flu. The deterioration of clinical condition was rapidly progressive and led to multi-organ failure. This includes severe and life threatening pneumonia,  which required intubation and ventilation, and acute kidney injury that necessitated continuous renal replacement therapy with high medical attention in the intensive care unit. The risk of life threatening scenario of 2009 H1N1 influenza is increased with young age, obesity, pregnancy, chronic medical conditions and decreased immunity.  Our patient was obese (body mass index of 35), but had no history of cardiovascular disease, diabetes mellitus, bronchial asthma or chronic kidney disease and he was not immune compromised or taking any drugs/ medications.
The early suspicion, recognition, and diagnosis of H1N1 in this patient has largely contributed to early intervention and management that resulted in full recovery. This reflects the increased awareness of medical and nursing staff that has been achieved by continuous education, repeated presentations and distribution of educational materials about signs and symptoms besides ways of early detection and diagnosis of 2009 H1N1. Furthermore, the H1N1 educational program reinforced the importance of taking all precautions and preventive measures and strict implementation of infection control policies and procedures, in order to avoid contamination and dissemination of infection, which prevented other patients and involved medical staff from contracting the 2009 H1N1 flu.
Acute kidney injury is expected in patients with sepsis and multi-organ failure, and early intervention with renal replacement therapy is crucial for stabilization of clinical condition and in achieving favorable outcome. , CRRT in the form of hemofiltration or hemodiafiltration has been shown to provide more hemodynamic stability, than classic hemodialysis, in critically ill patients in ICU; , though it might not have survival benefit over daily intermittent renal replacement therapy.  However, CRRT modality can be performed in an isolated room, where isolation of such patients is necessary, using a portable CRRT machine with disposable devices and sterilized dialysate and reconstitution fluids without the need of treated water or transferring patient to hemodialysis section, thereby avoiding exposure of other susceptible hemodialysis patients to H1N1 virus and the possibility of cross infection. Our patient received continuous hemodiafiltration over 180 hours which resulted in stabilization of his hemodynamic status, fluid balance, laboratory parameters and achievement of full renal function recovery.
Finally, prophylaxis with influenza vaccination reduces the frequency of influenza-like illness  and is associated with a lower risk of hospitalization and death in renal patients.  Two recent studies have described the effectiveness of two vaccines (adjuvanted and non adjuvanted) against the 2009 H1N1. , It has recently been shown, in a large prospective study, that influenza vaccination (against H1N1 and H3N2) confers high seroprotection (81%87%) in hemodialysis,  and peritoneal dialysis patients,  which is similar to healthy volunteers and where booster dose does not improve seroprotection rate, and seroresponse rates are not influenced by nutritional status, dialysis adequacy or uremic toxins.  Therefore, vaccination against 2009 H1N1 virus can help in protecting dialysis patients or at least minimize the severity of 2009 H1N1 infection. , Vaccination of health care providers, who are potential transmitters of influenza to others, is also important.  It remains, however, that implementation of infection control policies and procedures constitutes an essential part in protection against 2009 H1N1 and in particular in immune compromised patients. ,,,
Antiviral drugs (neuralminidase inhibitors) are effective in treating or reducing the severity of signs and symptoms of the 2009 H1N1. 
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