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Hamman’s crunch; a pathognomonic sign of pneumomediastinum. | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 28 September 2025 V1 Latest version Share on Hamman’s crunch; a pathognomonic sign of pneumomediastinum. Authors : Sophie McCullagh [email protected] , Carola Daniel 0000-0002-4801-5151 , John Keen 0000-0002-7862-5321 , Nicholas Parkinson 0000-0001-6336-5654 , and Bruce McGorum 0000-0002-6977-6101 Authors Info & Affiliations https://doi.org/10.22541/au.175908969.94985401/v1 430 views 211 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Pneumomediastinum, particularly spontaneous pneumomediastinum, is uncommon and presents a diagnostic challenge. In human medicine, auscultation of Hamman’s crunch, a crepitant, crunching noise, audible over the cardiac region in synchrony with the heartbeat, is considered pathognomonic for pneumomediastinum. This case report is the first to highlight the diagnostic utility of Hamman’s crunch for the diagnosis of pneumomediastinum in a horse. The horse’s clinical presentation differed from that of reported equine spontaneous pneumomediastinum cases, with pleurodynia (thoracic pain) and odynophagia (pain when swallowing) being prominent features. The investigation to confirm pneumomediastinum, identify potential underlying causes and rule out potentially fatal complications is described. The favourable outcome of this case is consistent with previous reports that spontaneous pneumomediastinum in the horse has a good prognosis, despite having dramatic presenting symptoms. CASE REPORT Hamman’s crunch; a pathognomonic sign of pneumomediastinum. Running title; pneumomediastinum Sophie McCullagh, Carola R. Daniel, John A. Keen, Nicholas J. Parkinson and Bruce C. McGorum Royal (Dick) School of Veterinary Studies and The Roslin Institute, University of Edinburgh, Roslin, UK Correspondence: Sophie McCullagh, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, UK. Email: [email protected] Royal (Dick) School of Veterinary Studies ORCID Sophie McCullagh https://orcid.org/0009-0005-3327-5275 Carola R. Daniel https://orcid.org/0000-0002-4801-5151 John A. Keen https://orcid.org/0000-0002-7862-5321 Nicholas J. Parkinson https://orcid.org/0000-0001-6336-5654 Bruce C. McGorum https://orcid.org/0000-0002-6977-6101 SUMMARY Pneumomediastinum, particularly spontaneous pneumomediastinum, is uncommon and presents a diagnostic challenge. In human medicine, auscultation of Hamman’s crunch, a crepitant, crunching noise, audible over the cardiac region in synchrony with the heartbeat, is considered pathognomonic for pneumomediastinum. This case report is the first to highlight the diagnostic utility of Hamman’s crunch for the diagnosis of pneumomediastinum in a horse. The horse’s clinical presentation differed from that of reported equine spontaneous pneumomediastinum cases, with pleurodynia (thoracic pain) and odynophagia (pain when swallowing) being prominent features. The investigation to confirm pneumomediastinum, identify potential underlying causes and rule out potentially fatal complications is described. The favourable outcome of this case is consistent with previous reports that spontaneous pneumomediastinum in the horse has a good prognosis, despite having dramatic presenting symptoms. KEY WORDS ; horse, spontaneous pneumomediastinum, pneumomediastinum, Hamman’s crunch INTRODUCTION Pneumomediastinum is defined as the presence of air or gas within the mediastinum. Three different mechanisms can produce pneumomediastinum; (1) leakage of air or gas through a breach in the airway, oesophagus, gastrointestinal viscus or tracking of air through an axillary wound, (2) gas produced by bacteria in the mediastinum, or (3) rupture of alveoli as occurs in spontaneous pneumomediastinum (Murayama 2014; López-Figueroa et al. 2024). Equine pneumomediastinum is described secondary to blunt or penetrating thoracic trauma, axillary and neck wounds, tracheal or oesophageal perforation and sinoscopy (Laverty et al. 1996, Boy and Sweeney 2000, Rojman et al. 2009, Joswig and Hardy 2013, Kruger and Davis 2013). There are only three reported cases of equine spontaneous pneumomediastinum in which no inciting cause was identified despite thorough examination (Smith and Marr 2019). Diagnosis of pneumomediastinum, particularly spontaneous pneumomediastinum, can present a diagnostic challenge. Up to 30% of cases of human spontaneous pneumomediastinum may go initially undiagnosed due to the vague nature of presenting symptoms (Sahni et al. 2013). This report highlights the diagnostic utility of auscultating Hamman’s Crunch, a crepitant, crunching noise, audible over the cardiac region in synchrony with the heartbeat in a horse with spontaneous pneumomediastinum. Hamman’s Crunch is considered to be pathognomonic for pneumomediastinum in human beings, although it is detected in only 11-18% of patients (Sahni et al. 2013, Alemu et al. 2021). The three previously reported cases of spontaneous pneumomediastinum presented with sudden-onset tachypnoea, fast shallow breathing, pyrexia, quiet demeanour and reduced appetite (Smith and Marr 2019), whilst pleurodynia and odynophagia (pain when swallowing) were additional prominent features in the present case. . CASE DETAILS Case history A 487kg 9-year-old Warmblood gelding was referred to the XXX (blinded for review) investigation of suspected equine grass sickness (EGS). The horse had been grazing during the daytime and had moved fields recently. He had been show jumping without an apparent problem earlier that day. Twenty hours prior to referral, the horse was recumbent in the field, appeared distressed and painful, with increased respiratory effort, generalised sweating, marked muscle fasciculations, reduced appetite, tachycardia (80 beats/min), quiet gut sounds and partial penile prolapse. The horse pawed the water bucket and water ran out of the mouth when drinking. There was a partial improvement in clinical signs following flunixin administration but continued tachycardia (60 beats/min) prompted referral for further investigation and treatment. Clinical and ancillary diagnostic findings at presentation On arrival, the horse was agitated, had a facial grimace, dilated nostrils (grade 4/4 nostril flaring; (Robinson et al. 2000)) and marked generalised muscle tremors. The tremors were more marked when the horse was anxious and reduced following sedation. Pain score was 3/3, based on a simple descriptive scale (0, none; 1, mild pain; 2, moderate pain; 3, severe pain). There was bilateral ptosis, patchy sweating, patchy piloerection, partial penile prolapse, and a tucked-up abdomen. The horse adopted a base-narrow stance and rested the hind quarters against the stable wall. He was normothermic, tachycardic (80 beats/min), had a fast (72 breaths/min) shallow breathing pattern with tacky mucous membranes and reduced abdominal borborygmi. The horse was sedated with xylazine (0.3mg/kg i.v.) to facilitate further examination; this reduced the severity of the marked generalised muscle tremors, which had hampered examination. There was a positive response to topical ocular application of 0.5% phenylephrine eye drops, suggestive of EGS (Hahn and Mayhew 2000). Abdominal ultrasonography and per rectum examination were unremarkable. Nasogastric intubation did not yield reflux. A venous blood sample showed an increased packed cell volume (50%) and total plasma protein (90g/L) and a stress leucogram. Routine biochemical analysis was unremarkable, except for increased serum concentrations of creatinine (150 µmol/l) and urea (10.9 mmol/l). Blood lactate concentration was 0.7mmol/L. Serum amyloid A concentration was 0mg/L, suggestive of no active inflammation. A provisional diagnosis of EGS was made. The horse was hospitalised and given intravenous Hartmann’s solution at twice maintenance rate, flunixin (1.1mg/kg i.v. bid for 4 days) and trickle fed grass. Clinical progress and definitive diagnosis of pneumomediastinum On re-examination three hours later, pleurodynia (thoracic pain) was evident on thoracic percussion, and when the horse was walking, moving and posturing to defaecate. The horse had notable odynophagia (pain and distress when swallowing). Pain score was 3/3. After sedation, when the severity of tremors had reduced, cardiac auscultation revealed a Hamman’s crunch over the heart on the right, and to a lesser degree, left side (Supplementary Audio File 1). This prompted a definitive diagnosis of pneumomediastinum. Palpation of the whole horse revealed a subtle, discrete area (approximately 10cm in diameter) of emphysema within the fascial planes of the right axilla at the 4th-5th intercostal spaces. There was no evidence of an underlying traumatic injury, although palpation of the thorax was resented. Pneumomediastinum was confirmed by radiography which revealed relatively broad linear rims of gas opacity outlining the trachea, aortic arch, cranial and caudal vena cava and oesophagus (Figure 1). Radiography did not identify rib fractures, pneumothorax or pulmonary lesions. Ultrasonography identified shred artefacts indicative of gas within the fascial planes adjacent to the trachea and blood vessels at the thoracic inlet, especially on the right side (Figure 2; Supplementary files 2 and 3). Auscultation, percussion, radiography and ultrasonography ruled out pneumothorax. Ultrasonography ruled out pneumopericardium, injured ribs and lesions of the pleurae and lungs. Endoscopy of the oesophagus, stomach and airway to the level of the major bronchi was unremarkable. Plasma ionised calcium concentration was within the reference range, indicating that the marked muscle tremors were not attributable to hypocalcaemia. Arterial blood gas analysis revealed PaO 2 82 mmHg, PaCO 2 46 mmHg and SaO 2 of 95%. As there was only mild hypoxaemia, provision of supplementary intranasal oxygen was not considered to be indicated. The horse had a spontaneous pneumomediastinum, with no identified underlying cause. Case progress The following day, the horse was bright and alert, but appeared uncomfortable, with generalized muscle fasciculations, rapid breathing (52 breaths/min) with marked nostril flaring and a base-narrow stance. Palpation of the thorax was resented. There were improvements in pain score (2/3), nostril flaring score (2/4), appetite, heart rate (44 beats/min), packed cell volume (40%) and total plasma protein (64 g/L). Azotaemia had resolved. Hamman’s crunch was still audible, particularly on the right side, but resembled clicks rather than crepitus. While the emphysema at the right axilla was no longer palpable, ultrasonography revealed persistence of gas in the fascial planes at the thoracic inlet, especially on the right side. The horse was turned out to graze in a small pen. On day three, the horse was more comfortable. Careful palpation revealed, for the first time, discrete areas of emphysema at the thoracic inlet bilaterally but particularly on the right side. On day five, the horse was recumbent, very distressed, with marked pleurodynia (pain score 3/3) and generalised muscle tremors. Radiography and ultrasonography showed no apparent change in the severity of pneumomediastinum and fascial emphysema. The symptoms improved following administration of flunixin (1.1 mg/kg i.v.). On days six and seven, the horse had several transient episodes of discomfort with muscle fasciculations and obvious signs of distress, particularly while eating, but these responded rapidly to flunixin. The horse was clinically normal from day eight onwards. Repeat radiographs taken on day eleven showed resolution of the pneumomediastinum (Figure 3), prompting the horse to be discharged with advice to avoid ridden work for eight weeks prior to a gradual return to exercise. The horse was reported to be clinically healthy and back in ridden exercise at 15 months after discharge. DISCUSSION This report highlights the diagnostic utility of auscultating Hamman’s crunch for the diagnosis of equine pneumomediastinum. Indeed, prior to auscultation of Hamman’s crunch, a provisional diagnosis of EGS had been made, given the similarity of the horse’s clinical presentation with that of EGS. Auscultation of Hamman’s crunch indicated that this provisional diagnosis was incorrect and indicated a definitive diagnosis of pneumomediastinum. If Hamman’s crunch had not been detected, given the horse’s dramatic clinical signs, it is conceivable it could have been euthanised on humane grounds with an incorrect diagnosis of EGS. Hamman’s crunch was not detected during the first examination, possibly because it was absent, or because the marked generalised muscle tremors and tachypnoea significantly limited auscultation. Hamman’s crunch has not been previously reported in horses, and is considered to be an uncommon finding in human patients, with a reported prevalence of 11-18% (Sahni et al. 2013; Alemu et al. 2021). The crunch detected in this case differed from the friction rubs, fluid and tinkling sounds that were audible on cardiac auscultation in a horse with pneumopericarditis (Durando et al. 2006). Pneumopericardium was ruled out in the present case by ultrasonographic examination. The clinical presentation of this case differs from that of the three previously reported cases which presented with sudden-onset tachypnoea, fast shallow breathing, pyrexia, quiet demeanour and reduced appetite (Smith and Marr 2019). In the present case, pleurodynia and odynophagia (pain when swallowing) were prominent features, in addition to tachycardia with fast and shallow breathing, marked generalised muscle tremors, pain when moving, resentment of thoracic palpation and a base-narrow stance. Flunixin and xylazine appeared to improve the severity of pain. Chest pain is the most common presenting sign (58%) of spontaneous pneumomediastinum in man, while 11-18% have odynophagia (Sahni et al. 2013; Alemu et al. 2021). Odynophagia is likely attributable to the food bolus causing painful movement of emphysema within fascial planes around the oesophagus and at the thoracic inlet. Water running out of the horse’s mouth after drinking is suggestive of dysphagia which is reported in 10-18% of human patients with spontaneous pneumomediastinum (Sahni et al. 2013; Alemu et al. 2021). The diagnosis of pneumomediastinum prompted a thorough examination of the thorax, neck and forelimbs for evidence of external injury, rib fractures and crepitus. Small, subtle areas of emphysema were palpated within the fascial planes of the right axilla on day two and at the thoracic inlet on day three. Palpable emphysema was detected in only 1/3 horses (Smith and Marr 2019) and 32% of human beings (Caceres et al. 2008) with spontaneous pneumomediastinum. Ultrasonography was more sensitive than palpation for detecting air within the fascial planes of the thoracic inlet. Pneumomediastinum was further confirmed by identifying characteristic features on thoracic radiographs. In the cases reported by Smith & Marr (2019), radiographic evidence of pneumomediastinum was subtle at the time of admission, but became more apparent over the following 48 hours. Given that mediastinal air was apparent on admission in only 69% of human patients with spontaneous pneumomediastinum (Caceres et al. 2008), computed tomography is the gold standard for diagnosis in people. Ultrasonography cannot visualise the mediastinum, due to the surrounding aerated lungs (Prange 2015). The present case, and the three reported by Smith & Marr (2019), were categorised as cases of spontaneous pneumomediastinum because no underlying cause of pneumomediastinum was identified despite thorough examination. It is important to attempt to identify an underlying cause given that some of the potential causes of pneumomediastinum, such as oesophageal rupture, carry a guarded prognosis. Clinical examination, thoracic radiography and ultrasonography, and endoscopy of the respiratory tract, oesophagus and stomach, ruled out potential causes of secondary pneumomediastinum including penetrating injuries of the thorax, trachea and sinuses, rib fractures, oesophageal perforation, axillary wounds and pulmonary disease. In hindsight, given that Smith & Marr (2019) considered pulmonary disease to be a potential cause of spontaneous pneumomediastinum in 3/3 horses, tracheal aspirate cytology could have been indicated. Collection and analysis of bronchoalveolar lavage fluid was, conversely, likely contraindicated given that this procedure commonly causes forceful coughing which could exacerbate alveolar injury. The aforementioned examinations also ruled out complications of pneumomediastinum including pneumothorax, pneumoperitoneum and pneumorrhachis (air within the spinal canal). Spontaneous pneumomediastinum occurs when alveoli or distal airways rupture due to a sudden increase in transmural pressure gradient. The lower pressure within the mediastinum than in the pulmonary parenchyma aids movement of air from the pulmonary interstitium via the bronchovascular sheaths to the pulmonary hila and into the mediastinum. Thereafter air may move into fascial plans in the neck, face, axillae, proximal limbs and thoracic wall, and into the pleural and peritoneal cavities and spinal epidural space (Macklin and Macklin 1944; Alemu et al. 2021, López-Figueroa et al. 2024). Potential precipitating factors for human spontaneous pneumomediastinum were identified in 41% of patients, including athletic activities (13%), cough (13%), snorting (6%), severe retching or vomiting (6%), childbirth (1%) and sneezing (1%) (Alemu et al. 2021). Given that the horse had been showjumping prior to the onset of clinical abnormalities, it is possible that this athletic activity could have caused alveolar injury leading to pneumomediastinum. As with human patients, the management of equine pneumomediastinum involves a conservative approach, potentially with oxygen supplementation, analgesia and avoidance of strenuous physical activity (Alexandre et al. 2018). The favourable outcome in this case supports a previous report (Smith and Marr 2019) which suggests that equine spontaneous pneumomediastinum cases make a rapid and complete recovery, despite the severity of the initial clinical signs. The prognosis in humans is similarly good, and because recurrence is considered unlikely, long-term follow-up examinations are not indicated (Alemu et al. 2021). In contrast to previous equine cases, and some human cases, the present case had no evidence of an acute inflammatory response, as assessed by rectal temperature, leucocyte counts and serum amyloid A concentration. Pyrexia and inflammation have been attributable to an inflammatory response to air within tissues or an underlying pulmonary disease (Caceres et al. 2008, Smith and Marr 2019). In summary, this case highlights the diagnostic utility of Hamman’s crunch for the diagnosis of pneumomediastinum in horses, and particularly for spontaneous cases. Despite the dramatic clinical presentation, equine spontaneous pneumomediastinum is associated with a good prognosis. AUTHOR CONTRIBUTIONS All authors contributed to case management and preparation of the manuscript and gave their final approval of the manuscript. ACKNOWLEDGEMENTS SM is a Horserace Betting Levy Board Senior Clinical Training Scholar. The authors thank the referring veterinary surgeons and owner. CONFLICT OF INTEREST STATEMENT The authors declare no conflict of interest. INFORMED CONSENT Informed consent was obtained from the horse’s owner. FUNDING N/a. Figure 1; Latero-lateral radiographs of the cranial thorax on day 1 after admission showing delineation of the major vessels with linear gas opacity (arrows). There is also gas around the thoracic trachea and oesophagus. A aorta, CVC caudal vena cava, D diaphragm, H heart, O oesophagus, PA pulmonary artery, PV pulmonary vein. Figure 2; Ultrasonograms taken at the thoracic inlet showing shred artefacts due to gas surrounding the great vessels within the cervical fascial planes. . Figure 3; Latero-lateral radiographs of the cranial thorax taken on day 11 showing resolution of pneumomediastinum (compare with Figure 1). Supplementary File 1 & 2; Audio clips recorded over the horse’s heart on day 2. Hamman’s crunch is audible, although it is not as clear as heard in real-time, particularly on Day 1. The sound quality is better if played through headphones. Supplementary File 3 & 4; US videos of shred artefacts References Alemu, B.N., Yeheyis, E.T. and Tiruneh, A.G. (2021) Spontaneous primary pneumomediastinum: is it always benign? J Med Case Reports 15 , 157.Alexandre, A.R., Marto, N.F. and Raimundo, P. (2018) Hamman’s crunch: a forgotten clue to the diagnosis of spontaneous pneumomediastinum. BMJ Case Reports 2018 , bcr-2018-225099.Boy, M.G. and Sweeney, C.R. (2000) Pneumothorax in horses: 40 cases (1980–1997). javma 216 , 1955–1959.Caceres, M., Ali, S.Z., Braud, R., Weiman, D. and Garrett, H.E. (2008) Spontaneous pneumomediastinum: a comparative study and review of the literature. Ann Thorac Surg 86 , 962–966.Durando, M.M., Zarucco, L., Schaer, T.P., Ross, M. and Reef, V.B. (2006) Pneumopericardium in a horse secondary to sternal bone marrow aspiration. Equine Veterinary Education 18 , 75–79.Hahn, C.N. and Mayhew, I.G. (2000) Phenylephrine eyedrops as a diagnostic test in equine grass sickness. Veterinary Record 147 , 603–606.Joswig, A. and Hardy, J. (2013) Axillary wounds in horses and the development of subcutaneous emphysema, pneumomediastinum and pneumothorax. Equine Veterinary Education 25 , 139–143.Kruger, K. and Davis, J.L. (2013) Management and complications associated with treatment of cervical oesophageal perforations in horses. Equine Veterinary Education 25 , 247–255.Laverty, S., Lavoie, J. ‐P., Pascoe, J.R. and Ducharme, N. (1996) Penetrating wounds of the thorax in 15 horses. Equine Veterinary Journal 28 , 220–224.López-Figueroa, C., Domingo, M., Duignan, P.J., Cuvertoret-Sanz, M., Martí-García, B., Pintado, E., Martinez, M. and Martínez, J. (2024) Air leak syndrome in animals: definition and pathogenesis. Journal of Comparative Pathology 211 , 42–51.Macklin, M.T. and Macklin, C.C. 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Equine Veterinary Education 21 , 621–626.Sahni, S., Verma, S., Grullon, J., Esquire, A., Patel, P. and Talwar, A. (2013) Spontaneous pneumomediastinum: time for consensus. N Am J Med Sci 5 , 460–464.Smith, S. and Marr, C.M. (2019) Spontaneous pneumomediastinum in three adult horses. Vet Record Case Reports 7 , e000732. Information & Authors Information Version history V1 Version 1 28 September 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keywords hamman’s crunch horse pneumomediastinum spontaneous pneumomediastinum Authors Affiliations Sophie McCullagh [email protected] The University of Edinburgh Royal Dick School of Veterinary Studies View all articles by this author Carola Daniel 0000-0002-4801-5151 The University of Edinburgh Royal Dick School of Veterinary Studies View all articles by this author John Keen 0000-0002-7862-5321 The University of Edinburgh Royal Dick School of Veterinary Studies View all articles by this author Nicholas Parkinson 0000-0001-6336-5654 The University of Edinburgh Royal Dick School of Veterinary Studies View all articles by this author Bruce McGorum 0000-0002-6977-6101 The University of Edinburgh Royal Dick School of Veterinary Studies View all articles by this author Metrics & Citations Metrics Article Usage 430 views 211 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Sophie McCullagh, Carola Daniel, John Keen, et al. 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