Intended for healthcare professionals

Endgames Case review

Dyspnoea after home improvement work

BMJ 2016; 355 doi: (Published 30 November 2016) Cite this as: BMJ 2016;355:i5957
  1. Alessio Marra, internal medicine resident,
  2. Nicoletta Bottero, internal medicine resident,
  3. Giovanna Leoncini, assistant professor,
  4. Giovanni Murialdo, professor
  1. Department of Internal Medicine, IRCCS AOU San Martino-IST, University of Genova, Genova, Italy
  1. Correspondence to A Marra dott.alessio.marra{at}

A 73 year old white man presented to the emergency department after unintentional ingestion of paraffin, which he had used as a paint remover two hours earlier. The episode was followed by cough, and the patient reported self induced vomiting. On admission he was eupnoeic and his respiratory rate, oxygen saturation, blood pressure, heart rate, and skin temperature were normal. The patient was a moderate smoker (15 cigarettes/day), and his history was notable only for a minor stroke two years previously without persistent sensory motor impairment. Physical examination, laboratory tests, and chest radiography were normal. No mucosal lesion was evident on an urgent gastroscopy. He was given vaseline oil and oral antacids. After 18 hours he developed hyperpyrexia (39°C), acute dyspnoea with desaturation (peripheral oxygen saturation 91% while breathing ambient air), and productive cough with blood streaks. A pulmonary examination identified fine crackles at the right lung base. White blood cell count and C reactive protein levels were increased (23×109/L (reference values: 4.5-9.8×109/L) and 216 mg/L (reference value: <5 mg/L) respectively). Contrast enhanced computed tomography (CT) of the chest was performed (fig 1).


Fig 1 Computed tomography scan of the lung


  • 1. What does the CT scan show and what is the diagnosis?

  • 2. How would you manage this patient?

  • 3. What extrapulmonary complications can arise?


1. What does the CT scan show and what is the diagnosis?

Short answer

The CT scan shows left pleural effusion and bilateral pulmonary infiltrates with consolidations, mixed with areas of low density involving the right middle lobe and the lingual (fig 2), suggestive of acute lipoid pneumonia. The diagnosis is paraffin ingestion related pneumonia.


Fig 2 CT scan shows bilateral lung consolidation (arrows) and left pleural effusion (*). Areas of low fat attenuation are visible in the context of infiltrates (arrowheads)


Multiple areas of reduced tomographic density (Hounsfield Unit (HU) values between−40 and−70)—better seen using a mediastinal window (fig 3)—are present in the midst of the infiltrates, consistent with low fat attenuation. Some reactive enlarged lymph nodes are present in the mediastinum (fig 4). All these findings are suggestive of acute lipoid pneumonia.


Fig 3 CT scan (mediastinal window) shows low fat attenuation inside the pulmonary infiltrates (arrows)


Fig 4 CT scan (mediastinal window) shows multiple reactive lymphadenopathy (arrows)

Paraffin ingestion related pneumonia occurs in 51-80% of paraffin intoxications.1 It is a form of lipoid pneumonia2 caused by aspiration and accumulation of fat-like compounds.3 Most lipoid pneumonias are chronic, secondary to longstanding low dose exposure to noxious agents (petroleum jelly, oily nasal drops, oil based laxatives, lip balm, gloss).3 However, acute forms related to massive inhalation of substances containing lipid can also develop. Paraffin intoxication is usually unintentional, sometimes work related, and only rarely related to suicide intent. Children are more exposed, especially in developing countries. 6 8

Many patients remain asymptomatic2; however, paraffin’s low viscosity, surface tension, and high volatility can lead to aspiration even when it is drunk. Agitation, cough, and vomit can increase the risk of aspiration. Paraffin can destroy alveolar surfactant and lung epithelium, 4 and in just one hour this can cause bronchiolitis, alveolar haemorrhage, and oedema. Desquamation of type II pneumocytes, fibrinoid leucocytosis, and microabscesses are usually seen in 24 hours.5 Collapse of alveoli and peripheral bronchioles may cause atelectasis, with subsequent ventilation or perfusion mismatch and hypoxaemia.6 Paraffin can also be excreted in the lungs from systemic circulation after gastrointestinal absorption, with detrimental effects on lung vasculature and function.7 Consolidation, pleural effusion, and pneumatoceles can develop in the first days and might persist for 4-6 weeks.8 Pneumothorax, bronchiopleural fistula,9 and pneumomediastinum10 have also been described. Fibrosis and restrictive pulmonary disease might develop in later stages,11 although most patients recover without sequelae. Development of acute respiratory distress syndrome is rare.12 Fever might be present, without secondary bacterial superinfection,13 which is uncommon in acute cases; however, deterioration 24 to 48 hours after ingestion is suggestive of superinfection.1 A chest radiograph has low diagnostic accuracy, but a high resolution CT scan is highly sensitive, and areas of low fat attenuation (HU−30 to 150) are characteristic. The anterior segments are commonly involved because of the “bending over” movement that follows ingestion and/or aspiration. 4 Diagnosis may be strengthened by lipid laden macrophages in sputum or in bronchoalveolar lavage fluid.2 3

Mortality is thought to be 0.2-0.5%.14 15 16

2. How would you manage this patient?

Short answer

General supportive care is the mainstay of treatment, and systemic corticosteroids, antibiotics, and inhaled bronchodilators can be used.


Vital signs (blood pressure, heart rate, respiratory rate, temperature, peripheral oxygen saturation, and level of consciousness) should be closely monitored, especially in the first 6-8 hours. Complete blood count is useful to check leucocyte levels. Despite the lack of data, use of C reactive protein levels to monitor the inflammatory process seems reasonable. Arterial gas analysis is indicated in the presence of desaturation. Electrocardiographic monitoring is useful in the first hours after exposure, owing to the increased risk of arrhythmias.17

Induction of emesis is contraindicated because of the extremely high risk of aspiration.18 Gastric lavage should only be considered in massive ingestions, within one hour, after airways have been secured with orotracheal intubation.17 Activated charcoal and whole bowel irrigation are ineffective.18 Catharsis is contraindicated. Early discharge for patients who are asymptomatic after six hours of observation has been suggested,11 18 19 even if respiratory symptoms develop slowly. Patients with symptoms require admission to hospital, given the possibility of rapid deterioration.17 20 Oxygen supplementation should be used as necessary and patients with acute respiratory distress syndrome might benefit from continuous positive airways pressure or non-invasive ventilation.17 Use of systemic corticosteroids in uncomplicated chemical pneumonitis is still debated: they might be helpful in reducing inflammation and subsequent fibrosis, but could, in theory, favour superinfections.11 13 15 18 21 Inhaled bronchodilators might be used safely in patients with wheeze.18 Differentiating bacterial superinfection from acute chemical pneumonia is challenging, and routine use of antimicrobial agents is controversial. Some case reports showed full recovery without steroids or antibiotics21; however, broad spectrum antibiotics can be used, even as prophylaxis,11 if clinical conditions worsen after 48-72 hours.1 13 Evidence suggests clinical outcome and length of hospital stay are similar, irrespective of prophylactic antibiotic treatment.22 There are no specific indications for bronchoscopic lung lavage but it could be reserved for acute severe cases or chronic conditions with severe functional impairment.12 23 In conclusion, at present clinical judgment and careful monitoring should guide management. Steroid and antibiotics might be reserved for patients of extreme age with concomitant cardiovascular or lung conditions, or with comorbidities.

3. What extrapulmonary complications can arise?

Short answer

Complications usually include gastrointestinal and neurological effects and, rarely, cardiac arrhythmias.


In addition to respiratory complications, gastrointestinal, neurological, and arrhythmias can develop.

Vomiting, a risk factor for aspiration, usually occurs in one third to one half of patients.24 Bloating, abdominal pain, and nausea are also common, whereas diarrhoea, haematemesis, and melaena are less so.17 They are secondary to local inflammation and usually transient. The potential for gastrointestinal mucosal damage is low; hence upper endoscopy is not routinely indicated if there is no upper gastrointestinal bleeding.

The central nervous system might be affected in around 5% of patients. This might manifest as lethargy, irritability, restlessness, ataxia, or drowsiness25; convulsions and, seldom, coma and death might also occur.17 The development of neurological manifestations correlates with the severity of pulmonary involvement, suggesting these are mainly due to hypoxia rather than a direct toxic effect. This could be related to the ability of liver and lungs to filter out large amounts of paraffin, protecting the brain.26

Cardiac arrhythmias, secondary to hydrocarbon sensitisation of myocardial cells to catecholamine, might occur17 19 but are more common in intoxication involving other hydrocarbons.17 Both neurological and cardiac manifestations (especially sudden cardiac death) are more common if paraffin or its vapours are inhaled.17

No specific treatment is available for the above complications; they usually respond to supportive care.17 19

As paraffin ingestion is considered the unintentional cause of most intoxications, every effort should be made to reduce the risk of exposure in work places or at home, where paraffin should not be stored in bottles intended for edible fluids and should be out of children’s reach.1 27 Fire eaters and people working in close contact with paraffin must be aware of the associated risk.

Patient outcome

The patient was transferred to the internal medicine department and given intravenous antimicrobial treatment with piperacillin/tazobactam 4.5 g three times daily. After three days of persistent fever, vancomycin 1 g twice daily and intravenous corticosteroids were added. After 14 days of treatment, the patient was discharged, and oral steroids were gradually tapered. All microbiological tests yielded negative results, and sputum was inadequate for lipid laden macrophages testing. Six weeks later, a follow-up CT showed almost complete resolution of infiltrates, with little fibrotic evolution. No residual pleural effusions or lymphadenopathy was evident (fig 5).


Fig 5 Six week follow-up CT scan showing minimal residual lung infiltration (arrow) and fibrotic evolution (*)

The patient is now well, without reported respiratory symptoms.


  • Competing interests: We have read and understood BMJ policy on declaration of interests and declare no competing interests.

  • Provenance and peer review: Not commissioned; externally peer reviewed.

  • Patient consent obtained.


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