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 Table of Contents  
POSTGRADUATE FORUM
Year : 2022  |  Volume : 2  |  Issue : 1  |  Page : 35-38

Young lady with respiratory failure


Department of Respiratory Medicine, Amrita Institute of Medical Sciences, Amrita Vishwa Vidya Peetham, Kochi, Kerala, India

Date of Submission24-Aug-2021
Date of Decision21-Sep-2021
Date of Acceptance21-Sep-2021
Date of Web Publication17-Jan-2022

Correspondence Address:
Dr. Nithya Haridas
Guddy's, Chittayil House, Vaduthala, Kochi, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jalh.jalh_19_21

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  Abstract 


Respiratory failure in a young adult presenting with community-acquired pneumonia usually suggests a diagnosis of acute respiratory distress syndrome (ARDS). Here, we discuss the case of a young female with pneumonia whose respiratory failure persisted despite treatment of pneumonia and ARDS.

Keywords: Mycoplasma pneumoniae, pleural effusion, pulmonary embolism


How to cite this article:
Haridas N, Mehta A, Kunoor A, George R. Young lady with respiratory failure. J Adv Lung Health 2022;2:35-8

How to cite this URL:
Haridas N, Mehta A, Kunoor A, George R. Young lady with respiratory failure. J Adv Lung Health [serial online] 2022 [cited 2022 May 16];2:35-8. Available from: http://www.jalh.com/text.asp?2022/2/1/35/335923




  Case History and Clinical Examination Top


A 26-year-old female, with no known comorbidities, came with the complaints of cough, fever, myalgia, headache, and diarrhea for 3 days. Cough was productive with minimal mucopurulent expectoration. She had left-sided pleuritic chest pain. There was no history of wheezing, hemoptysis, breathlessness, joint pain, rashes, hematuria, palpitation, and paroxysmal nocturnal dyspnea. She was admitted at an outside hospital for 2 days and referred to our center.

On examination, she was conscious, oriented, febrile (temperature-103.4 F), had tachypnea (respiratory rate of 36/min), tachycardia (pulse rate 124/min), blood pressure of 120/70 mm of Hg with oxygen saturation of 83% in room air. Her saturation improved to 98% with 4 l/min of supplemental oxygen. Her respiratory system examination revealed mid to late inspiratory crepitations in bilateral infra scapular areas. Breath sounds were decreased in left Infra axillary areas. Cardiovascular system, central nervous system, and gastrointestinal system examination were unremarkable.


  Management Top


SARS CoV 2 antigen and reverse transcription polymerase chain reaction (PCR) was negative. Hemogram on admission was unremarkable except for leukocytosis (total count of 12300/Cu. mm) with neutrophil 87.55%.

Her inflammatory markers were elevated with C-reactive protein of 312 mg/L and procalcitonin of 8.59 ng/ml. Her liver function, renal function test, and serum electrolytes at admission were normal. Arterial blood gas on admission showed pH of 7.50 with Pa CO2 of 26.4, Pa O2 of 61.6 SaO2 of 94.1%, HCO3-of 20.7, and lactate 1.1 at FiO2 of 0.37. [Figure 1] shows the chest radiograph at the time of admission.
Figure 1: Chest radiograph showing bilateral lower zone homogenous shadow which was more on left side with blunting of left costo phrenic angle

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Task 1: What could be the probable diagnosis?

  1. Diffuse alveolar hemorrhage
  2. Lobar pneumonia
  3. Viral pneumonia
  4. Aspiration pneumonia.


Answer: Diffuse alveolar hemorrhage is unlikely in the absence of hemoptysis. Moreover, her hemoglobin level was normal. Aspiration pneumonia may be excluded considering a young patient with absence of comorbidities or any history of seizures. A lobar pneumonia may be considered in view of acute course with high temperature and presence of effusion. However, a bilateral involvement with clinical picture suggestive of acute respiratory distress syndrome (ARDS) favors a viral pneumonia.

Her pao2/Fi O2 ratio was 157. She was admitted to intensive care unit and started on broad spectrum antibiotics (amoxicillin clavulanic acid and levofloxacin) antiviral (tab. oseltamivir) She was started on supplemental oxygen via nasal prongs. She was on prophylactic dose of low molecular weight heparin (LMWH) considering the possibility of pulmonary embolism in hospitalized patients. Her cultures, both sputum and blood, were negative for any growth. Ultrasound chest showed bilateral pleural effusion which was more on the left side. 450 ml of straw colored pleural fluid was aspirated from left pleural cavity after withholding LMWH for 12 hours. Pleural fluid analysis revealed exudative fluid, with pleural fluid lactate dehydrogenase (LDH) of 1117 IU/L and serum LDH of 547 U/L. Pleural fluid total WBC count was 1100 cells/cu. mm with differential counts showing predominantly lymphocytes.Pleural fluid ADA was 30.4 IU/L. Pleural fluid Gram smear and culture was negative. Pleural fluid mycobacterium tuberculosis PCR was negative.

Task 2: What are the investigation for atypical pneumonia?

  1. Throat swab for viral influenza PCR
  2. Urinary antigen for legionella
  3. Immunoglobulin M (IgM) and immunoglobulin G for Legionella pneumophila, Mycoplasma pneumoniae, and Chlamydophila pneumoniae.
  4. All the above.


Answer-D: All the investigations are to be send when you are suspecting an atypical pneumonia.

The first line investigations when you suspect an atypical pneumonia include chest radiograph, leucocyte count, hemoglobin level, liver function test, renal function test, oxygen saturation in air, and real-time reverse transcriptase polymerase chain reaction for SARS-CoV-2. The other investigations to be considered are urinary legionella antigen, sputum culture for legionella, molecular diagnosis for Chlamydia pneumoniae or mycoplasma pneumonia (MP), serology for atypical pathogens, and nasopharyngeal culture.

In view of clinical suspicion of viral pneumonia, throat swab was sent for PCR for H1N1 which came as negative. Serology showed mycoplasma IgM positive (0.395 U/ml). Her cold agglutinins were positive (4+). Her fever and radiological shadow improved with antibiotics, but her oxygen saturation remained low–88% on room air.

Task 3: Which investigation would you order next?

  1. D-dimer
  2. Computed tomography pulmonary angiogram (CTPA)
  3. Pulmonary function test
  4. Anit nuclear antibody (ANA) profile.


Answer-A D-Dimer

D-dimer levels have a high negative predictive values to rule out pulmonary thromboembolism. A negative result will help in ruling out pulmonary embolism. However, D-dimer levels can be raised in pregnancy, inflammation, malignancy, trauma, liver diseases, heart disease, postsurgical treatment, and prolonged hospitalization. CTPA is the gold standard for diagnosis of pulmonary thromboembolism.

In a patient with a history of progressive breathlessness, pulmonary function test including spirometry, lung volumes, and diffusion capacity for carbon monoxide would help to rule out restrictive lung disease. Connective tissue disease-related interstitial lung disease has to be ruled out in a patient with history of progressive breathlessness with hypoxia. Rheumatoid factor, anticyclic citrulinated peptide antibody, ANA profile are few investigations which will help to rule out connective tissue diseases in such patients.

Here, our patient does not have any history of comorbidities. She presented with a short duration of symptoms. Hence, an underlying pulmonary embolism was considered as a possibility and a D-dimer was ordered.

D-dimer level was 12.8 mcg/ml. As the patient was hospitalized for more than 1 week, positive predictive value of D-dimer was low in this case. Hence, a CT pulmonary angiogram was done to rule out pulmonary thromboembolism.

CT pulmonary angiogram [Figure 2] revealed multiple irregular filling defects noted in the apical and posterior segmental branches of the right superior pulmonary artery, segmental branches of the right inferior pulmonary artery, anterior segmental branch of the left superior pulmonary artery, and lateral basal segmental branch of the left inferior pulmonary artery. Bilateral lower limb arterial and venous Doppler was done and there was no evidence of any thrombus. She was initiated on anticoagulation with LMWH. Her oxygen saturation improved after starting therapeutic dose of LMWH. Her oxygen saturation was 97% on room air at the time of discharge. LMWH changed to warfarin at discharge maintaining the INR in the therapeutic range.
Figure 2: Computed tomography pulmonary angiogram showing irregular filling defects noted in the posterior segmental branches of the right superior pulmonary artery

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Task 4: What would be the ideal duration of anticoagulation?

  1. 3 months
  2. 6 months
  3. 12 months
  4. Indefinitely.


Answer: 3 months of anticoagulation is recommended for patients without cancer presenting with provoked pulmonary embolism.

She was continued on warfarin for 3 months. Repeat CTPA at 3 month showed complete resolution of thrombus.


  Discussion Top


MP is the second most common organism causing community-acquired pneumonia in young adults after streptococcus pneumonia.[1] The population at risk includes young adults and college students. It most commonly presents in the form of respiratory disease, but is also associated with a variety of extrapulmonary manifestations[2] MP is a common respiratory pathogen that produces diseases of varied severity ranging from mild upper respiratory tract infection to severe atypical pneumonia.

Common risk factors associated with M. pneumoniae include extremes of age, immunocompromising conditions like HIV, chemotherapy or steroids, or smokers with lung disease.[3] M. pneumoniae infection can present with a variety of symptoms, including cough, sore throat, vomiting, diarrhea, ear pain, articular pain, and myalgia. Serious pulmonary manifestations include pleural effusions, pneumothorax, pulmonary embolism. and interstitial pneumonitis. Extrapulmonary abnormalities seen in Mycoplasma infection include hemolysis, rashes, polyarthralgia, myalgia, bullous myringitis, encephalitis, meningitis, hepatitis, myocarditis, and glomerulonephritis.[4],[5] Rare complications associated with M. pneumoniae infection include ARDS, hemophagocytic syndrome, Stevens-Johnson syndrome, and disseminated intravascular coagulation[6]

This patient presented with one of the rare pulmonary complications of MP infection, namely, pulmonary embolism. Various hypotheses have been proposed for the possible mechanism of pulmonary embolism in mycoplasma infection. Mycoplasma is hypothesized to travel to the pulmonary artery and induce an inflammatory response with cytokines like interleukin-8 and tumor necrosis factor alpha, which will in turn cause vascular wall damage.[7] MP causes a hypercoagulable state through indirect mechanism. The antibodies created in response to Mycoplasma infection form immune complexes which cause an inflammatory response in the pulmonary arteries leading to endothelial damage and subsequent release of procoagulants.[7] Mycoplasma is also thought to increase the activity of human mononuclear cells' procoagulant activity.[7]

This patient had pleural effusion also. The effusion in this case could be either associated with pulmonary embolism or a parapneumonic effusion associated with M. pneumoniae pneumonia. Retrospective study done by Kim showed ratio of serum LDH to pleural fluid adenosine deaminase more than 7.5 favors Mycoplasma infection related paraneumonic effusion. This patient has a serum LDH of 547U/L and pleural fluid adenosine deaminase level was 30.4 IU/L, so the ratio is 14, favoring MP related parapneumonic effusion (MPPPE).[8]

MPPPE, one of uncommon feature of Mycoplasma infection, occurs in 4–20% of cases.[9],[10],[11] It usually presents as a lymphocytic exudative effusion with elevated adenosine deaminase (ADA) levels mimicking tuberculous pleural effusion.[12] Differentiation from tuberculosis is important in countries with high TB prevalence.

Though some complications of MP infection are life threatening, early identification and treatment can lead to a complete recovery.


  Conclusion Top


Respiratory failure in a young adult can have causes beyond ARDS. When respiratory failure persists, we should keep a high index of suspicion for unusual complications for common infections like mycoplasm pneumonia infection.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kashyap S, Sarkar M. Mycoplasma pneumonia: Clinical features and management. Lung India 2010;27:75-85.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Narita M. Classification of extrapulmonary manifestations due to Mycoplasma pneumoniae infection on the basis of possible pathogenesis. Front Microbiol 2016;7:23.  Back to cited text no. 2
    
3.
Klement E, Talkington DF, Wasserzug O, Kayouf R. Identification of risk factors for infection in an outbreak of Mycoplasma pneumoniae respiratory tract disease. Clin Infect Dis 2006;43:1239-45.  Back to cited text no. 3
    
4.
Lieberman D, Schlaeffer F, Lieberman D, Horowitz S, Horovitz O, Porath A. Mycoplasma pneumoniae community-acquired pneumonia: A review of 101 hospitalized adult patients. Respiration 1996;63:261-6.  Back to cited text no. 4
    
5.
Liong T, Lee KL, Poon YS, Lam SY. Extra pulmonary involvement associated with Mycoplasma pneumoniae infection. Hong Kong Med J 2015;21:569-72.  Back to cited text no. 5
    
6.
Chan ED, Welsh CH. Fulminant Mycoplasma pneumoniae pneumonia. West J Med 1995;162:133-42.  Back to cited text no. 6
    
7.
Huang Z, Zhang B, Cheng B. Mycoplasma pneumoniae pneumonia complicated with pulmonary embolism: A systematic analysis of published case reports. ICEM 2016;9:11574-81.  Back to cited text no. 7
    
8.
Kim CH. Usefulness of serum lactate dehydrogenase/pleural fluid adenosine deaminase ratio for differentiating Mycoplasma pneumoniae parapneumonic effusion and tuberculous pleural effusion. J Infect 2017;75:581-97.  Back to cited text no. 8
    
9.
Suzuyama Y, Iwasaki H, Izumikawa K, Hara K. Clinical complications of Mycoplasma pneumoniae disease – Other organs. Yale J Biol Med 1983;56:487-91.  Back to cited text no. 9
    
10.
Fine NL, Smith LR, Sheedy PF. Frequency of pleural effusions in mycoplasma and viral pneumonias. N Engl J Med 1970;283:790-3.  Back to cited text no. 10
    
11.
Linz DH, Tolle SW, Elliot DL. Mycoplasma pneumoniae pneumonia. Experience at a referral center. West J Med 1984;140:895-900.  Back to cited text no. 11
    
12.
Cha SI, Shin KM, Jeon KN, Yoo SS, Lee J, Lee SY, et al. Clinical relevance and characteristics of pleural effusion in patients with Mycoplasma pneumoniae pneumonia. Scand J Infect Dis 2012;44:793-7.  Back to cited text no. 12
    


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  [Figure 1], [Figure 2]



 

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