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| CASE REPORT |
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| Year : 2021 | Volume
: 10
| Issue : 3 | Page : 209-211 |
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A fatal typhoid acute respiratory distress syndrome: Report of a rare case
Fahmi Yousef Khan1, Elmukhtar M Habas2, Raza Ali Akbar1, Theeb Osama Sulaiman2
1 Department of Medicine, Hamad General Hospital; Weill Cornell Medical College, Doha, Qatar
2 Department of Medicine, Hamad General Hospital, Doha, Qatar
| Date of Submission | 16-Aug-2021 |
| Date of Acceptance | 01-Sep-2021 |
| Date of Web Publication | 6-Dec-2021 |
Correspondence Address:
Fahmi Yousef Khan
Department of Medicine, Hamad General Hospital, Doha, Qatar. Weill Cornell Medical College/Qatar, P.O. Box: 3050, Doha
Qatar
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/sjhs.sjhs_117_21
We report a fatal case of typhoid acute respiratory distress syndrome (ARDS) in a 32-year-old man who was hospitalized with fever, cough, and chills lasting 12 days. While waiting for the results of cultures, his condition rapidly deteriorated within 2 days, and he developed ARDS. The patient was transferred to the medical intensive care unit. Subsequently, his blood, urine, and stool cultures returned positive for Salmonella Typhi. The sensitivities showed that the organism was resistant to nalidixic acid, ampicillin, and ciprofloxacin but was sensitive to ceftriaxone. The patient was intubated, and mechanical ventilation was initiated, while ceftriaxone, vasoactive amines, and hydrocortisone were administered. Unfortunately, the patient died despite escalation to intensive care and the care provided thereof. This interesting case was selected from our previous study entitled Epidemiological and Clinical Features of Salmonella Typhi Infection Among Adult Patients in Qatar: A hospital-based study. Different aspects of typhoid ARDS including clinical presentation, pathogenesis, diagnosis, and treatment are discussed and the literature has been reviewed.
Keywords: Acute respiratory distress syndrome, ceftriaxone, ciprofloxacin, typhoid fever
How to cite this article:
Khan FY, Habas EM, Akbar RA, Sulaiman TO. A fatal typhoid acute respiratory distress syndrome: Report of a rare case. Saudi J Health Sci 2021;10:209-11 |
| Introduction | |  |
Typhoid fever is a systemic disease caused by Salmonella enterica serotype Typhi. It remains a significant public health problem, especially in developing countries, where sanitary conditions are poor and population's access to clean drinking water is limited.[1],[2] This acute illness usually manifests with quite non-specific symptoms which are clinically indistinguishable from other febrile illnesses, making early diagnosis harder. Although it is a treatable condition, a delay in the diagnosis may lead to serious complications and even death.[3] Major complications include intestinal hemorrhage, intestinal perforation, cholecystitis, myocarditis, and pneumonia.[2],[3],[4],[5],[6] Acute respiratory distress syndrome (ARDS) is an extremely rare complication of typhoid fever. A review of the literature revealed a few case reports attributed to ARDS.[7],[8],[9],[10],[11]
In this report, we present a fatal case of typhoid ARDS most probably attributed to a delayed diagnosis. Through this case report, we aim to increase the awareness of health-care providers about the fatal consequences of delays in the diagnosis of typhoid fever and to highlight the importance of keeping a high index of suspicion for an early diagnosis to prevent such lethal consequences.
| Case History | | |
A 32-year-old Bangladeshi man was admitted to the hospital with fever, cough, and chills. His illness started 12 days prior to presentation as a simple fever, for which he received paracetamol. Two days later, he developed frequent watery, nonbloody diarrhea; therefore, he went to a private clinic where he was prescribed oral ciprofloxacin treatment. In the following days, his diarrhea subsided, but the fever continued. He also now developed a cough. The patient went back to the same private clinic where he underwent investigations. His completel blood count, peripheral smears for malaria parasite, urine microscopy, and blood chemistry were carried out and were unremarkable. The patient was prescribed an oral course of amoxicillin/clavulanic acid and was sent home. Subsequently, the patient's condition deteriorated as, despite medications, his fever, cough, and chills continued and he developed shortness of breath. At this point, he presented to our hospital where he was admitted. The patient's other past medical history was unremarkable. He had come from Bangladesh to Qatar 1 month ago.
His clinical examination on admission to the emergency department revealed that he looked ill, though being fully conscious, alert, and oriented. His vital signs revealed a temperature of 38.8°C, blood pressure (BP) of 110/60 mmHg, pulse rate of 110 beats/min, and respiratory rate of 24 breaths/min. There were no skin rashes, petechiae, or ecchymoses. The neck was supple, without jugular venous distension or lymphadenopathy. His chest and abdominal examinations were unremarkable as was the rest of his systemic examination.
The laboratory investigations revealed a hemoglobin level of 11.0 g/dL, a total leukocyte count of 5400/mm3 with a normal differential, and a platelet count of 98,000/mm3. Blood chemistry, liver profile, and coagulation studies were within normal limits. A malarial parasite smear was negative, and the urine dipstick only showed +1 leukocytes. Blood, urine, and stool cultures were sent to the laboratory.
Based on the clinical presentation and the history of recent travel to Bangladesh, enteric fever was suspected and the patient was admitted to the medical ward for further workup and management. Ceftriaxone 2 g intravenously once daily was started while laboratory studies were pending. During hospitalization, tuberculin skin test and human immunodeficiency virus enzyme-linked immunosorbent assay were done which were negative. His Widal test returned positive. The ultrasound scan of his abdomen was unremarkable.
On the 2nd day after admission, the patient developed sudden breathing difficulties, which rapidly precipitated to respiratory distress. On examination, he was sick and dyspneic but conscious. His BP was 90/60 mmHg. Auscultation of his chest revealed widespread coarse crepitations bilaterally. His plasma B-type natriuretic peptide value was 110 pg/mL, and a chest X-ray showed bilateral diffuse and symmetric pulmonary infiltrates. Transthoracic echocardiography showed right ventricular dysfunction with an ejection fraction of 55%. Based on these findings, the patient was diagnosed with ARDS and was transferred to the medical intensive care unit (MICU). The oxygen saturation in the blood continued to be inadequate despite the initial noninvasive ventilatory support. Around the same time, blood, urine, and stool cultures yielded S. Typhi which was resistant to nalidixic acid, ampicillin, and ciprofloxacin but sensitive to ceftriaxone. The patient was intubated, and mechanical ventilation was initiated, while ceftriaxone, vasoactive amines, and hydrocortisone were administered. Despite all these aggressive supportive measures in MICU, unfortunately, the patient could not survive.
| Discussion | | |
The pathogenesis of extraintestinal infectious complications of typhoid fever depends on the ingested inoculum size, virulence of the strain, the host's immune response, previous exposure, and local protective factors.[12] S. Typhi enters the bloodstream causing transient bacteremia which is rapidly cleared as bacilli are phagocytosed by the macrophages and monocytes of the reticuloendothelial system. Viable bacilli within the reticuloendothelial system multiply and re-enter the bloodstream causing bacteremia for several days and weeks known as secondary bacteremia, during which all the organs are repeatedly exposed to S. Typhi and localized infection may occur at any site due to hematogenous dissemination.[12],[13]
Lung involvement in typhoid fever has been less commonly reported. It occurs in <20% of the cases in the form of bronchitis, pneumonia, lung abscess, empyema, and rarely ARDS,[9] which is mainly found in immunocompromised patients with AIDS, leukemia, Hodgkin's disease, sarcoidosis, and kidney transplant patients.[9],[10],[11] Patients at extremes of age (children, elderly) are also at high risk of developing such complications.[9],[10],[11] In contrast to this norm, we described an immunocompetent patient with typhoid fever who developed ARDS without any evidence of immunosuppression and rapidly deteriorated despite maximal support.
ARDS is an acute-onset, life-threatening condition characterized by poor oxygenation and bilateral pulmonary infiltrates, in the absence of any evidence of cardiogenic pulmonary edema.[14] It should be noted that many patients with acute respiratory failure from ARDS also develop nonpulmonary organ failure, such as cardiovascular failure requiring vasopressor support.[15] The diagnosis of ARDS in our patient is based on the sudden deterioration of his clinical condition, poor oxygenation, bilateral pulmonary infiltrates, and normal cardiac ejection fraction. However, during respiratory failure, our patient developed cardiovascular failure and required vasopressor support.
ARDS is a rare and potentially fatal complication of typhoid infection. So far, the knowledge about its pathogenesis is limited. It has been suggested that Salmonella can cause lung damage by activating the contact system, leading to massive red blood cell infiltration and the deposition of fibrin in the infected lungs.[16] Other investigators have proposed that endotoxemia induces an increase in alveolar–capillary permeability, which leads to the development of alveolar edema and proteinosis.[8],[14],[17] Another likely mechanism of ARDS in a patient with enteric fever could be that in severe sepsis, the high burden of pro-inflammatory cytokines such as tumor necrosis factor, interleukin-1 (IL-1), IL-6, and IL-8 can lead to an acute lung injury that progresses to ARDS resulting in respiratory failure.[18] Regardless of the underlying etiology and the proposed mechanism, ARDS goes through various phases, beginning with damage to the alveolar–capillary, a proliferative phase characterized by improved lung function and healing, and a final fibrotic phase that signals the end of the acute disease process.[14],[15]
Isolation of S. Typhi is required to confirm the diagnosis of the disease. Blood cultures are positive in 40%–80% of patients, stool cultures in around 30%–40%, and bone marrow cultures in approximately 90% of the cases.[19] Bone marrow culture is the most sensitive diagnostic tool, especially in complicated cases or when antimicrobial therapy has already been initiated and the diagnosis remains uncertain, as it can be positive in up to 50% of patients after a maximum of 5 days of prior antimicrobial therapy.[9] In our patient, blood, urine, and stool cultures were all positive, reflecting widely disseminated S. Typhi.
Prompt administration of relevant antibiotic therapy protects from severe typhoid complications. However, the antibiotic treatment of typhoid fever faces enormous challenges due to the development and rapid spread of Salmonella resistant to first-line antimicrobials such as ampicillin, trimethoprim–sulfamethoxazole, and in recent years, fluoroquinolones. Therefore, local antimicrobial guidelines should be followed at the earliest in treating such cases to avoid any delays in the initiation of appropriate treatment. In the state of Qatar, a previous study showed ceftriaxone to be the empirical treatment of choice for suspected cases of typhoid fever while awaiting sensitivity results.[20] Likewise, in our case, S. Typhi was resistant to ciprofloxacin and ampicillin but susceptible to ceftriaxone. Unfortunately, our patient presented quite late to our hospital and developed ARDS most probably as a result of receiving inadequate treatment prior to this admission. We believe that this patient was a victim of the ignorance of the clinicians in the private centers of the causative bacteria or the reported efficacy of different antimicrobials against typhoid fever. The role of steroids in treating typhoid ARDS is controversial since there are no guidelines. However, one case report showed the effectiveness of dexamethasone in improving the outcome in one patient.[11]
| Conclusion | | |
ARDS is a rare complication of typhoid fever which can occur as a result of late diagnosis and/or delayed administration of relevant antibiotics. Clinicians should be aware of this life-threatening presentation of typhoid fever and of the locally reported efficacy of different antimicrobials against this infection. Both these measures can lead to the establishment of an early diagnosis and initiation of timely treatment to prevent the grave life-threatening consequences of this infection in case of delay.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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