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END STAGE RENAL FAILURE WITH SUSPECTED TUBERCULOSIS AND HOSPITAL ACQUIRED PNEUMONIA.

Byline: Hadeer Akram Abdulrazzaq Raja Ahsan Aftab Amer Hayat Khan Azhar Amir Hamzah Nurul Jannah Ambak and Azreen Syazril Adnan

ABSTRACT: Immunocompromised chronic kidney disease (CKD) patients are often subjected to multiple complications. Hospital Acquired Pneumonia (HAP) is common among patient with long term warded in hospital. A 56 years old Malay women diagnosed with end stage renal failure 2 years ago was presented with intermittent fever and on/off cough with whitish sputum. Patient was admitted one week before for chest infection. The laboratory finding shows that the patient had hypochromic mycocytic anemia since her hemoglobin and hematocrit level was below normal range. The CT thorax done proposes a suggestive that the patient had chest infection or pneumonia. Chronic kidney disease patients are often associated with multiple co-morbidies. Low immune response makes CKD patients an ideal subject for hospital acquired pneumonia. Critical review on patient pharmacotherapy should be done in patients with conditions that alter drug pharmacokinetics as CKD.

Key words: chronic kidney disease hospital acquired pneumonia multiple co-morbidies

1. INTRODUCTION

End stage renal failure (ESRF) is last stage kidney disease

when estimated glomerular filtration rate is less than 15 mL/min/1.73m2 [1]. ESRF Patients at this stage will require renal replacement therapy in the form of dialysis or transplantation to sustain life. This disease is characterized by a progressive deterioration in kidney function that ultimately leads to irreversible kidney damage. Complication that associated with ESRF other than increase complexity of the condition is fluid and electrolyte abnormalities anemia cardiovascular disease hyperparathyroidism bone disease and malnutrition. Studies indicate that both innate and adaptive immune system contribute to an increased rate of infection among ESRD patients. Functional abnormalities of monocytes neutrophils and dendritic cells are directly linked with ESRD patients [2-4]. With so many medications prescribed to ESRD patient compliance or adherence issue become a major problem in most of the patient.

Hospital acquired pneumonia is defined as infection of the lungs that occurs greater than 48 hours after admission that was not incubating at the time of admission [5]. Tuberculosis is caused by M. tuberculosis an aerobic non-spore-forming bacillus often refered to as acid-fast bacillus (AFB). This disease usually spread through the air patient with low immune system will have high possibility to get infected. The symptom of TB is almost similar to pneumonia such as cough loss appetite coughing up blood or mucus weakness or fatigue fever and night sweats [5].

Case presentation

A 56 years old Malay women weighing 39Kg was admitted to Hospital Universiti Sains Malaysia (HUSM) with complaining of intermittent fever and on/off cough with whitish sputum. The patient had hemoptysis and complained of shortness of breath. She was admitted to the ward one week before for chest infection or pneumonia. Patient also claimed to have anemic symptom (pallor tremor nausea) before loss conscious at home. On examination subject had mild tachypneic and her vital sign were; BP (160/65mmHg) PR (100 bpm) RR (20 bpm) T (38.5OC) and saturated partial O2 (SPO2) are 92% under room air and 96% under Nasal Prongs O2 (table 1). Physical examination find that her lung presents with coarse crept at right side. Computed tomography (CT) thorax shows a multiple area of consolidation in keeping with chest infection.

Table 1: laboratory profile of patient

Laboratory###Patient###Normal range

profile###value

Hgb###7.5 g/dL###11.5-16.4 g/dL

Hct###23.6%###36-47%

Platelet###136 x103/L###150-400 x103/L

PO4###0.79###0.8-1.45

###mmol/L###mmol/L

Total Protein###58 g/L###66-83 g/L

Prothrombine###14.8s###10-13.5s

Time

aPTT###77.0s###26-42s

PCO2###116 mmol/L###35-45 mmol/L

HCO3###30 mmol/L###72-100 mmol/L

O2 Saturation###99%###90-95%

On admission patient was diagnosed with upper GI bleeding secondary to ureamicgastropathy end stage renal failure (ESRF) secondary to obstructive uropathy hospital acquired pneumonia and also with hypochromic mycocytic anemia. She was on regular hemodialysis (HD).

Multiple pharmacotherapies were initiated to stabilize the patient. Peptic ulcer disease (PUD) is a common reason for upper gastric bleeding patient was prescribed pantataperazole (40 mg BD) to treat PUD. Antihypertensive were also initiated to control bleeding disorder of GI this included enalapil (10mg BD) and felodipine (10mg OD). Antibiotics for hospital acuquired pneumonia was initiated that included azithromycin tazocin meropenem and voriconazole

The patient was treated for pneumonia along with other complications aggressively since her lab reports were improving and to avoid any further hospital acquired infection patient was discharged 4 days after the initiation of treatment and asked to take complete rest. Table 1 provides the details of medication prescribed to patient to improve her condition.

2. DISCUSSIONHospital acquired pneumonia (HAP) occurs due to the imbalance between host defenses and microbial propensity for colonization and invasion shift in favor to the ability of pathogens to persist and invade lower respiratory tract. The source of infection is from healthcare devices or the environment (air water equipment and fomites) and can occur with transfer of microorganisms between staff and patients [1].

In treating HAP third-generation cephalosporin broadspectrum penicillins fluoroquinolones aminoglycosides and carbapenems can be used as they provide broad-spectrum activity against the common aerobic pathogenscausing HAP. Other agents such as macrolides and lincosamides linezolid and vancomycin have excellent activity against Grampositive cocci while demonstrating minimal activity against Gram-negative bacilli [2]. In treating current patient the doctor prescribes azithromycin 500mg OD and IV piperacillin/tazobactam 225mg TDS then change to IV meropenem 500mg TDS. Piperacillin/tazobactam is the first choice in treating HAP which covers Pseudomonas and azithromycin is given to cover Legionella [3].

Table 2: medication given to patient in the ward

###Drug Name###Dose###Indication###Metabolism###Primary

###Regimen###Excretion

###T. Isoniazid###200mg OD###Anti-TB###Hepatic###Renal

###T. Rifampicin###300mg OD###PTB Smear -ve###Hepatic###Renal

###T. Pyrazinamide###750mg OD###Hepatic###Renal

###T. Ethambutol###800mg OD###Hepatic###Renal

###T. Pyridoxine###10mg OD###Hepatic###Renal

###T. Azithromycin###500mg OD###Antibiotic for HAP Hepatic###Hepatic

###IV Tazocin###225mg TDS###Hepatic###Renal

###IV Meropenem###500mg TDS###Hepatic###Renal

###IV Voriconazole###200mg BD###Hepatic###Renal

###T. Enalapil###10mg BD###Antihypertensive###Hepatic###Renal

###T. Felodipine###10mg OD###Hepatic###Renal

###T. Isordil###10mg TDS###Angina Pectoris###Hepatic###Renal

###T. Atovastatin###20mg ON###Hepatic###Renal

###T.###35mg BD###Hepatic###Renal

###TrimetazidineHCl

###(Vastarel MR)###0.5mg PRN###Hepatic###Renal

###T. Nitroglycerin

###T. Pantoprazole###40mg BD###PUD###Hepatic###Renal

###T.###10mg TDS###Antiemetic###Hepatic###Renal

###Metoclopramide

###(Maxolon)

###KCl mist###15mL TDS###Hypokalemia###-###-

###T. CaCO3###1mg TDS###Hyperphosphatemia###Hepatic###Hepatic

###in ESRD

###T. Folic Acid###5mg OD###Hematinic Agent###Hepatic###Renal

###T. Vitamin B###1/1 OD

###Complex###400mg OD

###T. Ferrous

###Fumarate

HAP can be divided into early-onset and late-onset HAP. Early-onset HAP happens within 4 days of admission and is often attributed to community-acquired organisms that were colonizing the patient around the time of hospital admission. Late-onset HAP (5 days or more) is more likely to be caused by more resistant gram-negative bacilli S. aureus including methicillin-resistant S. aureus (MRSA) and L. pneumophila [4]. According the guidelines for pneumonia in adult patients antipseudomonal AY-lactam plus an anti pseudomonal fluoroquinolone or aminoglycoside plus or minus linezolid or vancomycin for MRSA are the regimens for late onset of HAP [4]. Current patient was only prescribed meropenem for her HAP. Thus fluoroquinolone or aminoglycoside should be added to the regimen for HAP.

Tuberculosis (TB) can only been diagnosed by culturing M. tuberculosis organisms from a specimen taken from the patient. TB is difficult to diagnose due to the difficulty in culturing the slow-growing organism in the laboratory. A complete evaluation for TB includes a medical history a chest radiograph a physical examination and microbiologic smears and cultures. It may also include a tuberculin skin test and a serologic test. The first line treatment of tuberculosis is isoniazid rifampicin pyrazinamide ethambutol and streptomycin [5]. In this case the patient was given isoniazid 200mg stat then OD rifampicin 300mg stat then OD pyrazinamide 750mg stat then OD (except HD day) ethambutol 800mg stat then OD. Three specimen of sputum acid-fast bacilli (AFB) done in this patient showed negative result but the treatment was continued. This is because negative smear results do not exclude TB disease.

Culture of clinicalspecimens will confirm the diagnosis in smear-positive cases and usually identify that many cases since the culture is more sensitive (80 to 85%) compared to smear. However the time to detection and speciation of cultures may be up to 7 weeks particularly when the burden and metabolicactivity of the mycobacteria are very low as is often the case in smear-negative culture-positive disease [6]. The treatment was continued even with the AFB smear is negative as it takes some time waiting for the culture result.

Serum galactomannan was detected in this patient. Galactomannan is the molecule found in cell wall of aspergillus sp. Vorionazole is the drug of choice for primary therapy of most patients with aspergillosis as it provided improved survival and fewer side effects [7]. In patients with Clcrless than 50ml/min accumulation of IV vehicle (cyclodextrin) of voriconazole occurs. After initial IV loading dose oral voriconazole should be administered unless an assessment of benefit vs risk to the patient justifies the use of IV voriconazole. Serum creatinine should be monitored and changing to oral voriconazole therapy should be done when possible. QT prolongation has been associated with voriconazole use. Rare cases of arrhythmia cardiac arrest and sudden death have been reported usually in seriously ill patients with risk factors such as electrolyte imbalance. For current patient electrolyte abnormalities (hypokalemia hypomagnesemia hypocalcemia) should be corrected prior to initiating the therapy.

Rifampicin is contraindicated with the use of voriconazole. Rifampicin decreases the levels of voriconazole by increasing the metabolism. This problem can be encountered by adjusting the dosing interval 3-4 hours apart for the time taking anti-tuberculosis drugs and voriconazole.

3. CONCLUSION

CKD patients have alterations in their pharmacokinetic parameters such as drug absorption distribution protein binding biotransformation and renal function. Such patients are usually with multiple co-morbidities and require close observation. The role of clinical pharmacist in applying pharmacokinetics principle in dosage adjustment drug dosage adjustment monitoring and assessing patient medication therapy is critical.

4. REFERENCES

[1]. Chastre J. and J.-Y. Fagon Diagnosis of ventilatorassociated pneumonia. N Engl J Med 356(14): p. 1469 (2007).

[2]. Rotstein C. et al. Clinical practice guidelines for hospital-acquiredpneumoniaandventilatorassociated neumonia in adults. The Canadian JournalofInfectiousDiseasesandMedical Microbiology 19(1): p. 19 (2008).

[3]. Cunniffe J. K. Stirling and C. Sluman Wirral University Teaching Hospital Antimicrobial Formulary April2011. http://www.whnt.nhs.uk/document_uploads/IntranetPharmacy/Antibiotic%20formulary%20_March%2020 11_ae4da.pdf Accessed 2/4/2014.

[4]. Guidelines for the Management of Adults with Hospital-acquired Ventilator-associated and Healthcare-associated Pneumonia. Am J Respir Crit Care Med 171: p. 388416 (2005).

[5]. Espinal M.A. et al. Standard short-course chemotherapy for drug-resistant tuberculosis.JAMA: The Journal of the American Medical Association 283(19): p. 2537 (2000).

[6]. Long R. Smear-negative pulmonary tuberculosis in industrialized countries. CHEST Journal. 120(2): p. 330-334 (2001).

[7]. Dipiro J.T. and A. Pharmacotherapy Pathophysiologic Approach McGraw Hill Companies South Carolina (2008).
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Publication:Science International
Article Type:Report
Date:Sep 30, 2014
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