Introduction

A burn injury can be defined as a thermal injury where the temperature of the tissue (the skin commonly or any other organ) has exceeded the harmful level and the tissue gets damaged or dies. For the human skin, the pivotal temperature often mentioned is approximately 43 °C [1,2,3]. Also, the relationship between time and temperature is crucial [4, 5].

The term burn however includes several different types of injuries with different traumatogenesis that can be intentional or non-intentional. There are the obvious flame and contact burns, with the increased temperature as common denominator—not only thermal burns but also friction, chemical, radiation, and electrical burns. Even though these entities have different traumatogenesis and medical courses, the treatments are mainly parallel to the one of thermal burns.

A scald can be viewed as a certain type of contact burn even though they often are mentioned alone. A scald occurs when the skin (or other tissue/organ) comes in contact with hot steam or liquids. Many scalds occur at home and the majority involve the paediatric population [6]. Most scalds in the paediatric population are minor and can successfully be treated in an out-patient setting; scalds can however occur in all ages. Steam inhalation therapy, vide infra, sometimes causes scalds and a number of cases have been reported during the last decades [7,8,9,10].

Inhaled steam, or hot air, is usually effectively cooled off in the airways, why thermal damage is rarely seen below the glottis. Explosive combustion and presence of hot steam,—especially if induced with pressure or during an inhalation/gasp—can create a situation where the capacity of cooling down the inhaled air is exceeded and thermal inhalation injury occurs even below the glottis. Scalds in the facial region should increase the suspicion of inhalation of hot air/liquid.

The, since long, used steam inhalation therapy is supposed to treat/prevent upper respiratory tract infections (URTI) as common cold or bronchiolitis. Steam inhalation therapy was recommended as early as 1926 by the Surgical Catalogue, to be used with water pipes or kettles for inhalation [11]. This briefly helps a blocked nose but shows no curative effect on common colds according to a Cochrane review [12]. Reports of scald injuries related to steam inhalation therapy have, however, been described in numerous papers, rarely involvement of the respiratory tract is seen. [7,8,9,10, 13,14,15,16,17,18,19,20,21,22].

Pathophysiology of steam burns and steam inhalation injuries

Inhalation injury is a broad term that includes tissue damage as well as systemic toxic effects due to inspiration of steam or combustion products such as smoke and its contained chemicals. The presence of an inhalation injury can be suspected not only from the patient history, for example in the event of smoke exposure in an enclosed space, but also from clinical findings such as burns to the face and mucosa of the nose and mouth, as well as carbonaceous sputum and changes in the voice. Bronchoscopy is usually required to confirm the suspicion [23]. The definitive diagnosis, however, is somewhat subjective and requires an experienced clinician.

A concomitant inhalation injury is associated with a worse prognosis in burn patients, with longer hospital stay and higher mortality. The more extensive the burn is, the higher the risk of a concomitant inhalation injury. In patients with a burn extent < 20% total body surface area (TBSA), the prevalence of inhalation injury is approximately 2%. In patients with a burn extent > 80% TBSA, however, the prevalence is > 14% [24], in some reports as high as 85% [25, 26]. Difficulties in diagnosing inhalation injury likely contributes to the variation in reported prevalence. Three clinical types of inhalation injury exist (and can exist together):

Upper airway injury (above glottis)

Airways above the larynx, i.e. the uvula, pharynx, and epiglottis, are damaged. The tissues may swell considerably and thus this always involves the risk of acute total upper airway obstruction. Inhalation of hot gases, hot liquids, or chemicals is usually the traumatogenesis.

Lower airway injury (below glottis)

Epithelial damage, inflammation, abundant secretion, and obstruction occur when injurious substances reach below the larynx and the airway and lung parenchyma can be damaged.

Toxic effects

Inhalation of toxic gases results in more systemic effects. The scope of the damage depends on factors as, e.g. solubility and concentration of the toxic or noxious substances.

Smoke chemicals, larger particles, and hot air often injure the upper airways, while water-soluble materials and smaller particles often also cause damage more distally [27]. The mucosa of the airways is affected by steam similar to other tissue with the heat leading to denaturation of proteins causing complement activation leading to oedema [27]. The upper airway plays an important role in the conditioning of inspired air, in normal circumstances heating and humidifying it. Inhaling dry air, with a low capacity of maintaining heat, makes the upper airways act as a heat exchanger turning most gases to body temperature before they reach the lower airways [28, 29]. Steam, however, allows for inhalation of a greater amount of thermic energy resulting in the ability to transport steam further down the respiratory tract.

Smoke inhalation also increases the blood flow [30] associated with a change in permeability to proteins and small particles as well as changes in pressure conditions leading to inflammation and oedema. These factors together with a smooth muscle hyperreactivity [27] can lead to a life-threatening total obstruction of the lower airways [31, 32]. After the initial acute response, the more long-lasting effects are similar to those of a bronchopneumonia.

Inhalation of heated air with a high humidity, i.e. steam, specifically, is a topic that is less explored. Humid air cools, as formerly explained, slower than dry air/gas when passing down the airway, potentially leading to more heat reaching the lungs with humid hot air [29]. Moritz et al. describe that the heat transfer to the respiratory mucosa when inhaling 500 cc of dry air at 142 °C, assuming that it would be cooled to 38 °C at exhalation and would add up to around 13 cal of heat to the body. This is significantly less than the 200 cal that would be transferred when inhaling the same volume of a steam–air mixture at 125 °C, again assuming that the temperature at exhalations would be 38 °C [29]. In their experimental animal study from 1944, they describe that none of their subjects sustained pulmonary injury from the inhalation of oven-heated air. In the groups inhaling flames from a blast burner and steam, however, the rate of pulmonary injury was as high as 20% and 67%, respectively [29]. The most vulnerable part of the lung seems to be the central part of the parenchyma, due to the direct connection with the primary bronchi [29]. With extensive thermal injury, histopathological analysis shows a destruction of bronchial mucosa and haemorrhagic oedema of peripheral and central lung parenchyma [29]. Aviado et al. also described a rise in aortic blood temperature shortly after the inhalation of steam, reflecting the uptake of heat [33]. They also noted several other physiological changes, including an immediate apnoea and bradycardia followed after a minute by a polypnea and tachycardia [33].

Pathophysiology of cutaneous steam burns

The exact mechanism of skin damage during accidental exposure to steam is not fully understood. Cutaneous steam burns can be due to accidents related to direct contact, e.g. sudden explosions of steam pipes. Another cause of cutaneous steam burn described is when firefighters are exposed to external heat together with sweat in the clothing layers which start to evaporate, and a condensation process occurs on the skin. The condensation of the steam takes place on the colder environment on the skin then the heat of the vaporization of water is released, eventually leading to an increased temperature of the skin which can cause a cutaneous steam burn [34, 35]. The mechanism of the skin damage has been studied before, when exposed to dry heat [36] and hot water [37]. Less studies are found about cutaneous steam burns [38]. As described above, the protective clothing of firefighters and its mechanism with temperature water vapour diffusion has been studied thoroughly [34, 35, 39, 40]. Some believe that cutaneous steam burns are more severe than dry air, due to the dermis, which is damaged, without any significant indication of damage to the epidermal layer. This theory was confirmed by Zhai et al. [38] in an ex vivo porcine model, investigating the mechanisms of cutaneous steam burns and the response of the skin when in contact with high-temperature steam. It showed that the steam penetration in the porcine model damaged the dermis earlier than the epidermal layer, which could explain why cutaneous steam burns are usually more severe than dry heat burns to the skin [38].

Objective

This scoping review aims to conclude and summarize published papers in English about steam-related injuries and we present a clinical case of a 26-year-old man with severe steam inhalation injuries and cutaneous steam scalds.

Review

A search was conducted using the PubMed® and Cochrane libraries on 19th of May 2021, without a set time period. The search terms were synonyms of “steam”, “vapor”,” burns”, “inhalation injury”, “pulmonary insufficiency”, and “lung injury”. The exact search strategy used can be seen in Figs. 1 and 2. The total literature search identified 1198 articles written in English and after duplicates were removed, 1186 articles remained (Fig. 3). The papers were screened for relevance and eligibility. The inclusion criteria used were all papers describing a case, or cases, involving a steam inhalation injury or burn. A total of 31 articles were included and analysed based on year of publication, type of paper, number of patients involved, age, gender, type of injury/event, treatment, and outcome (Table 1).

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The search strategy on PubMed®

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Fig. 2
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The search strategy in the Cochrane Library

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Out of a total of 1186 identified records, 31 were chosen for review. Described more in detail in Table 1

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Table 1 Literature review of the 31 articles included, analysed based on year of publication, type of paper, number of patients involved, age, gender, type of injury/event, treatment, and outcome
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Case report

A 26-year-old man was referred to the Burn Centre at Uppsala University Hospital due to an extensive burn contracted while working on the central heating of his house. Due to a mechanical failure, there was a large explosion-like release of steam, within the enclosed quarters of his basement.

The initial assessment of the patient estimated that a mix of deep dermal to full-thickness burns covered 55% TBSA. The burns included face, upper and lower extremities, and the back (Fig. 4). The front of the trunk was surprisingly spared from injury (Fig. 5). There was no soot present in the mouth or pharynx; however, there were signs of damage to the buccal mucosa, most probably due to inhaled steam. The 26-year-old was intubated upon arrival to the referring hospital and subsequently promptly transported to our department. During transport, he was unstable and had no urine production despite receiving 15 l of crystalloid solutions (Ringer’s acetate) during the first 10 h, as well as a noradrenaline infusion.

Fig. 4
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Part of the estimated 55% (TBSA) burn on the face, back, upper and lower extremities

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Fig. 5
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The front of the trunk which was spared from the burns. The genitalia and the tattoo of the left hand are covered

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Upon arrival, fiberbronchoscopy showed redness similar to mucositis in the buccal mucosa, gingiva, tongue, and palate continuing down into the trachea. Escharotomy was performed on the forearms and hands due to circumferential burns, and enzymatic debridement (NexoBrid ®, MediWound Ltd, Israel) was initiated to treat the burns on the lower extremities.

On day 2, the patient was tachycardic with an acute renal failure and continuous renal replacement therapy (CRRT) was initiated. The following day (3), he deteriorated respiratory and circulatory with a greater need of continuous noradrenalin infusion, a metabolic acidosis, and a lactate of 5 mmol/l. During days 4 and 5, the patient recovered circulation, and the noradrenaline infusion was removed, but with respiratory worsening with increased O2-demands and increased PEEP of 14 cm H2O.

Excision of the burns on his hands and upper extremities as well as placement of a tracheostomy was done on day 6. Due to further respiratory deterioration, the patient was placed in prone position with a slight improvement. Muscle relaxation was used to handle CO2-retention and asynchronous breathing. On day 9 post admission, the plastic enclosure to the UniPerc® cannula (Smiths Medical Inc, MN, USA) of the tracheostomy was found broken and the inner canula was replaced using video laryngoscopy and a tube exchange guide wire due to the risk of accidental decannulation, in the presence of senior consultants from ENT and intensive care. At this point, a grayish white mucosa was noted in the pharynx and down to the laryngeal plane. Later the same evening and continuing to the next day (10), the patient continued to deteriorate with regard to respiratory parameters. Bronchoscopy was performed, showing a rift in the left side of the trachea at the outlet to the left main bronchus. Decision was made to initiate veno-arterial extracorporeal membrane oxygenation (VA-ECMO) treatment while placing a stent in the trachea and bronchus to cover the rift. After the stent, the same afternoon, the patient was moved from the burn ICU to the cardiothoracic ICU. Later that same afternoon, a flow of air from the nasogastric tube was noted as well as gastric contents in the tracheostomy. Bronchoscopy was again performed, showing a fistula from the left main bronchus to the oesophagus.

On day 11 post admission, a significant difference was seen in the oxygen saturation in the right arm when compared to the right foot, consistent with Harlequin syndrome [41] and a poor lung function. VA-ECMO was switched to veno-venous ECMO (VV-ECMO). Bronchoscopy at this point showed a satisfactory passage of air past the defect. Bronchial intubation was attempted bilaterally to increase oxygenation and an oesophageal stent was placed to decrease the contamination of the mediastinum. At this point, the ventilation of the right lung was successful, but despite this, in combination with ECMO treatment, the oxygen saturation was not satisfactory. The patient was severely unstable and suffering from multiorgan failure including renal and liver failure with hemolysis, disseminated intravascular coagulation (DIC), and sepsis. Even dressing changes were nearly impossible due the circulatory and respiratory deterioration when changing positions. At this point, a multidisciplinary team concluded that it was not possible to reverse the situation and saw no alternative for a long-term repair of the trachea even if supportive care was to be successful and the decision was made to switch to palliative care. The patient expired after 2 h.

At the autopsy, the burns previously described as well as remaining conditions after the previous treatment measures were confirmed.

During the internal examination, severely edematous organs were seen with thickening of the scalp as a result of the extensive resuscitation fluid therapy. Ordinary anatomical conditions were seen in the brain and the basal brain vessels.

Several discolorations were seen on the tongue, which in places were fibrin-coated, and a blood infiltration was noted in the tongue base. The upmost part of the epiglottis had a ragged tear in its frontal aspect (Fig. 6). Upon opening the oesophagus, at both limitations of the inserted stent (12.5 cm in length), transverse chafing-like lesions were seen in. Beneath the stent, a continuous lesion, measuring about 5 × 2.5 cm (L × W), communicating with the trachea was seen. Additionally, two longitudinal mucosal tears were noted in the oesophagus (Fig. 7).

Fig. 6
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The base of the tongue, the ragged epiglottis (↑), and the pharynx seen from above, with severe, fibrin-coated, tissue damage in the mucosa (†)

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Fig. 7
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The opened esophagus showing the longitudinal lesion between the esophagus and trachea (*) with the breathing tube slightly visible just above the carina (↓), the transverse chafing-like lesions at both limitations of the stent (∆), and the longitudinal mucosal rift (†)

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The pleurae were shiny without adhesions or foreign material. The lungs were greatly increased in consistency, compact, and heparinized almost in the whole, with a weight > 1600 g each (normal approximately 500 g). At incision, a yellowish tissue with light clearings similar to broncho-lobular pneumonia was seen (Fig. 8). Stretching from the trachea down into the peripheral parts of the airways, a yellow-coloured, sometimes wounded, mucous membrane with varying depths of damage and occasional bleeding was seen in both lungs, with the cartilage rings completely unprotected in places showing laryngotracheobronchitis (Figs. 9 and 10). Corresponding to the tissue defect in the oesophagus, a similar defect was seen in the wall of the trachea just above the carina where the surrounding tissue was brittle and thin.

Fig. 8
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Signs of broncholobular pneumonia in the lungs with scattered foci of yellowish consolidation and a generally red and solid section (↑)

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Fig. 9
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The opened airways with severe mucosal damage and unprotected cartilage rings in the trachea (*). The lesion in the photography shows the place of the tracheostomy ( →)

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Fibrin-coated airways down into the peripheral parts of the lungs (↓)

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The heart was slightly enlarged (450 g, normal 350–400 g) but without obvious edematous appearance and no further pathology. The kidneys, spleen, pancreas, and adrenal glands were normal although edematous. The liver was fluid-filled with a rounded anterior edge, heavy (3050 g, normally approximately 1500 g), and had a grainy, buttery tissue at incision.

In the histopathological examination of the brain, hyperemic tissue was seen in the cerebrum. In the hippocampus, corresponding to the CA1 area, pycnotic, dark-coloured nuclei were seen, indicating acute oxygen deficiency. Regarding the lungs, tissue samples were taken from all lobes, the two main bronchi, the macroscopic haemorrhages in the two bronchi and from the trachea. In the left lung, the alveoli were almost completely filled with erythrocytes and neutrophilic granulocytes (Fig. 11). Hyaline membranes were also seen in several places as signs of acute respiratory distress syndrome/diffuse alveolar damage (ARDS/DAD) (Fig. 12). The mucosa of the left main bronchus was completely absent, and the underlying cartilage tissue was infiltrated by fungal growth with surrounding pus. In the right lung, a similar picture was noted with not only extensive acute inflammation and fungal growth in the cartilage parts but also several bleeding foci (Fig. 13). In the alveoli, fibrin was seen, as in late stages of pneumonia (Fig. 14). Several abscess formations were noted in the right lung (Fig. 15).

Fig. 11
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Lung tissue showing severe infiltration with neutrophil granulocytes (*) as well as erythrocytes (Δ) in the alveoli compatible with early stage of pneumonia (Hematoxylin–eosin, × 10)

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Fig. 12
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Lung tissue with formation of hyaline membranes (†) compatible with diffuse alveolar damage (DAD) as well as alveolar bleeding (Hematoxylin–eosin, × 10)

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Fig. 13
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Bronchial cartilage with fungal growth (‡) and surrounding neutrophil granulocytes (*) (Hematoxylin–eosin, × 10)

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Fig. 14
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Alveoli´s filled with fibrin (↑) compatible with late stage of pneumonia (Pikro-Mallory, × 10)

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Fig. 15
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Lung tissue with abscess formation (*) and surrounding alveolar bleedings (Δ) (Hematoxylin–eosin, × 4)

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All oesophageal tissue samples showed damaged mucosa and even deeper damage of the circular muscle layers in some sections. Acute inflammatory cells were mainly seen in the adventitia, compatible with mediastinitis.

Besides putrefactive transformations in the liver and kidneys, no abnormal histopathological findings were found.

In summary, the autopsy and subsequent histopathological examination showed extensive external burns, residual conditions after treatment with escharotomies, amputations, skin transplants, and edematous organs. Extensive mucosal damage was seen throughout the bronchial tree, the oesophagus, and the mouth, and discoloration and tissue defects were seen on the tongue and epiglottis. In the lungs, a bilateral pneumonia was seen where characteristics from all four classical stages could be found as well as signs of diffuse alveolar damage. The conclusion was that the death was due to the complications after extensive scalding injuries in the airways in combination with the tissue defect between the trachea and oesophagus. It is not completely clear if the defect between the trachea and oesophagus was due to the thermal damage or due to an iatrogenic injury caused on day 9 post admission, when they changed the UniPerc® cannula.

Discussion

Burns related to the contact with steam are generally rare and can be both minor and severe. The more severe cases related to steam exposure are mostly workplace accidents [50] and the minor injuries reported in the literature are often related to steam inhalation therapy, especially in the paediatric population [7,8,9,10, 13,14,15,16,17,18, 18,19,20,21,22].

Our literature review found 8 case reports, 13 case series, 8 reviews, and 2 letters to the Editor. We included a total of 31 papers in our review related to our inclusion criteria described above. The case reports/series described different cases ranging from steam inhalation therapy injuries with minor injuries to severe high-pressure steam burns with major injuries [7,8,9,10, 13,14,15,16,17,18,19,20,21,22, 42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58].

Hathaway et al. (1996) [48] have reported a case, with a similar mechanism of injury as in our current paper: a high-pressure steam pipe ruptured, and the patient sustained 60% TBSA burns with a steam inhalation injury. In both Hathaway et al.’s patient and ours, extensive mucosal damage was seen throughout the bronchial tree with severe necrotizing laryngotracheobronchitis, found in the autopsy. Below the glottis, this type of burns to the airway are rare unless inhalation of steam is involved [49]. In the case series by Brinkmann et al. (1978) [49], a steam tube on a ship exploded causing both cutaneous steam burns and severe steam inhalation injuries with similar pathological findings were described. In total, 27 men died, at different intervals. In the victims who died on the scene, coagulative necrosis could be found in the trachea, bronchial walls, and at the level of the lungs. The parenchyma of the lungs demonstrated oedema and desquamation of the alveoli and alveolar epithelial cells. These patients most probably died from acute pulmonary failure and shock. In the patients surviving the accident, some other complications were described: respiratory distress syndrome (RDS), desquamative interstitial pneumonia, and confluent bronchopneumonia. The macroscopical findings of the respiratory tract described the mucosa as “of greyish colour” and almost 50% had subpleural haemorrhages. Brinkmann et al. [49] concluded that the acute changes in these patients were due to severe lesions of the lungs and the alveolar-capillary membrane leading to hypoxia and shock.

Preventive measures to avoid the potential life-threatening situation with inhalation of high-temperature steam to the respiratory tract and death have been studied by the French Navy [46]. The exposure to this mechanism of injury is higher on nuclear ships or submarines and a laboratory was designed to study different protective equipment and fabrics. According to the French Navy, the study showed that water vapour impermeable garments had a better protection when it comes to steam exposure. The ventilator treatment in acute lung injury due to steam inhalation injuries has been studied in animals by Wang et al. (2006) [59], concluding that high-frequency oscillatory ventilation (HFOV) could be an optional treatment. According to this study, the HFOV stops the decrease in oxygenation and the compliance of the lungs and also decreases the inflammatory process and tissue damage in the lung.

Steam inhalation therapy has long been an accepted alternative treatment of upper respiratory tract infections (URTI). The earliest description of the dangerous and negative impact of steam inhalation therapy we found in our review dates back to 1972 [7], then later again described in 1981 [19], 1989 [16], and 1990 [13]. These three papers describe the underrecognized risk of scalding, especially in children when receiving humidified air to treat or prevent URTI. These scalds can be severe causing full-thickness burns, leading to surgery and skin grafts which lead to permanent scarring [15]. The cost can be high when dealing with steam inhalation scalds and most of these studies recommend an increased awareness of these scalds for future prevention [8, 9]. The retrospective review by Baartmans et al. (2012) [17] included 49 patients with burns related to steam inhalation therapy. It is proposed that steam inhalation therapy should not be used and considered as a dangerous procedure. This is due to the lack of proven benefit and the risk of serious complications as scalds.

Mass casualty events related to cutaneous steam burns and steam inhalation injuries have been described throughout history until present day [42, 44, 49, 51, 60, 61]. One of these events was included in our review by Tekin et al. (2005) [51] describing a boiler room steam explosion on board a cruise ship and injured 15 employees on the cruise ship. Of these 15 employees, 6 had severe cutaneous steam burns over 80% TBSA, together with steam inhalation injuries and all these patients unfortunately passed away.

Iatrogenic steam burns are generally rare; a case report by Choi H et al. (2016) [45] describes a 12-day-old infant at the neonate intensive care unit which presented with a deep dermal cutaneous steam burn to the nose due to a heated, humidified high‐flow nasal cannula (HHHFNC) with a failure when setting the temperature.

A tragic and rare event involving steam occurred in 2005 and is described by Bhootra et al. [22] and involves 2 children, 6 and 17 years old, who watched their mother inhale steam for her URTI; the older child accidently spilled the boiling water which caused a huge amount of steam in their enclosed room. According to the mother, the children started to struggle with their breathing within 1–2 min and both subsequently passed away. The autopsy showed microscopical injuries to the respiratory tract with inflammatory response, coagulative necrosis, lung congestion along with haemorrhages, and oedema.

Conclusions

This case and the literature review demonstrate the challenges that can be encountered when handling patients with cutaneous steam burns and/or steam inhalation injuries. A steam injury to the airways or the skin can be directly life-threatening due to its severity and should be treated with caution. Many studies highlight the danger of steam to the respiratory tract and its vulnerability to this type of injury that can lead to acute respiratory insufficiency and sometimes death. This is also demonstrated in the case report described above.