Renal parenchymal rupture,pelvic rupture and uroabdomen secondary to bilateral renal hemorrhage and pyelonephritis in a cat

Abstract

Case summary

An 8-month-old male castrated domestic shorthair cat was presented for acute stranguria, pollakiuria and vocalization. The patient was diagnosed with urethral obstruction and hospitalized for medical management. At 36 h after discharge, the cat started passing severely hemorrhagic urine and was diagnosed with a uroperitoneum and uroretroperitoneum. An abdominal ultrasound and fluoroscopic retrograde positive contrast cystourethrogram did not identify a source of urinary tract rupture. An exploratory laparotomy revealed urine leakage from both kidneys, with evidence of rupture involving both the renal pelvis and parenchyma. It is suspected that sterile pyelonephritis and renal hemorrhage resulted in bilateral ureteral obstruction, and subsequent uroretroperitoneum, extending to cause uroperitoneum. Left ureteronephrectomy and right subcutaneous ureteral bypass placement was offered as a salvage procedure; however, euthanasia was elected intraoperatively because of a poor prognosis.

Relevance and novel information

Renal pelvic and parenchymal rupture is a poorly reported cause of uroabdomen in the cat. Furthermore, although severe renal hemorrhage has not been described in cats, it may lead to bilateral ureteral obstruction and uroabdomen.

Keywords

Uroretroperitoneum uroperitoneum ureteral obstruction feline idiopathic cystitis renal hematuria

Introduction

Uroabdomen occurs after rupture of the urinary tract, with urine accumulation into the peritoneal cavity and/or retroperitoneal cavity. Uroperitoneum occurs as a result of rupture of the distal ureters, bladder or urethra, while uroretoperitoneum results from rupture of the kidneys or proximal ureters.¹ Renal rupture is an uncommon cause for uroabdomen, and is subclassified as a renal parenchymal, renal collecting system or mixed rupture in humans.² Renal parenchymal rupture typically results in retroperitoneal hemorrhage, either from ruptured renal neoplasms, renal calculi, pyelonephritis, vasculitis or pregnancy.^2–6 Renal collecting system rupture typically occurs after ureteral obstruction from ureteral calculi and results in uroretroperitoneum.^7–10 In cats, renal pelvic rupture has been reported after obstructive ureterolithiasis,¹¹ while renal parenchymal rupture has been reported secondarily to idiopathic renal lymphoplasmacytic inflammation¹² and ruptured perinephric pseudocysts.¹³ This case report describes a novel case of spontaneous renal rupture and uroabdomen, secondary to bilateral renal hemorrhage and pyelonephritis.

Case description

An 8-month-old male castrated domestic shorthair cat presented to the emergency department for stranguria, pollakiuria and vocalization. At 12 days prior, the cat presented to its primary veterinarian for hematuria, pollakiuria and dysuria, but did not have a urethral obstruction (UO). Bloodwork, urinalysis, urine culture and abdominal radiographs were performed (Tables 1 and 2). Gabapentin (10 mg/kg PO q8–12h), prazosin (0.5 mg PO q12h), robenacoxib (2 mg/kg PO q24h) and a Royal Canin Urinary SO diet were prescribed. Clinical signs resolved within 2 days.

Table 1

Blood results from the cat’s primary care visit (–12 days), first hospitalization (0 days), second hospitalization (2 days) and 14 h after admission (2.5 days)

Time (days)	–12 days	0 days (first admission)	2 days (second admission)	2.5 days (14 h after admission)	RI
Venous blood gas analysis
pH	–	–	7.253	7.234	7.352–7.450
pCO₂ (mmHg)	–	–	40.0	42.1	30–40
HCO₃^– (mmol/l)	–	–	17.3	17.4	18–26.3
Base excess (mmol/l)	–	–	−9.3	−9.6	−4 to 0
Na⁺ (mmol/l)	–	–	148.1	146.9	143.7–151.1
Cl^– (mmol/l)	–	–	101	99	109–117
K⁺ (mmol/l)	–	–	5.14	6.08	3.66–4.72
iCa⁺⁺ (mmol/l)	–	1.38	1.19	1.09	1.23–1.40
Anion gap (mmol/l)	–	16	35.0	36.6	11.6–21.1
Lactate (mmol/l)	–	–	2.56	0.95	0.43–2.10
Glucose (mg/dl)	–	283	275	208	70–115
PCV/TS
PCV (%)	–	48	39	32	–
TS (g/dl)	–	6.3	9.5	9.0	–
Selected CBC and chemistry values
Hematocrit (%)	43.4	–	39.3	–	–
Leukocytes (K/µl)	9.11	–	30.37	–	2.87–17.02
Neutrophils (K/µl)	6.61	–	11.43	–	2.30–10.29
Monocytes (K/µl)	0.25	–	1.05	–	0.05–0.67
Lymphocytes (K/µl)	1.91	–	17.29	–	0.92–6.88
Eosinophils (K/µl)	0.18	–	0.14	–	0.17–1.57
Platelet count (K/µl)	45* Manual: 260	–	37^†	–	151–600
Total protein (g/dl)	6.9	–	9.0	–	5.7–8.9
Albumin (g/dl)	3.2	–	3.2	–	2.2–4.0
Globulin (g/dl)	3.7	–	5.8	–	2.8–5.1
Creatinine (mg/dl)	0.7	1.0	9.5	8.5	0.8–2.4
BUN (mg/dl)	22	31	126	161	16–36
Phosphorus (mg/dl)	5.6		14.0	15.8	3.1–7.5
Potassium (mmol/l)	4.1	3.4	4.9	–	3.5–5.8
Sodium (mmol/l)	164	152	146	–	150–165
Chloride (mmol/l)	133	119	104	–	112–129
Total calcium (mg/dl)	9.4	–	10.2	–	7.8–11.3

The primary care veterinarian performed a manual platelet count as the automated count was below the reference interval (RI)

†

In-house automated complete blood count (CBC) was performed. Platelet clumping was detected by the machine; however, manual blood smear review was not performed

BUN = blood urea nitrogen; PCV = packed cell volume; TS = total solids

Table 2

Urinalysis results from the cat’s primary care visit (–12 days), first hospitalization (0 days) and second hospitalization (2 days)

Time (days)	–12 days	0 days (first admission)	2 days (second admission)
Gross appearance	Red, turbid	Yellow, cloudy	Red, cloudy
USG	1.038	1.046	1.012
pH	7.5	7.0	6.0
Urine protein	3+	2+	3+
Glucose	Negative	2+	Negative
Blood	3+	2+	3+
Bilirubin	Negative	Negative	1+
Ketones	Negative	Trace	Negative
WBC (/HPF)	0–2	0–2	0–2
RBC (/HPF)	>100	20–30	>100
Epithelial cells (/HPF)	0–1	0–1	3–5
Bacteria	None	None	None
Casts	None	None	None
Crystals	2+ struvite	1+ struvite	None
Urinary cystatin B (ng/ml) (RI <99)	–	<50	110
Aerobic urine culture	Negative	Negative	Negative

HPF = high power field; RBC = red blood cells; RI = reference interval; USG = urine specific gravity; WBC = white blood cells

On presentation to the emergency department, the cat was afebrile, stable and euhydrated and had a firm, moderate-sized bladder that was unable to be expressed. In-house bloodwork was performed (Table 1). Hydromorphone (0.05 mg/kg IM) and Normosol-R (4.4 ml/kg/h IV) were administered. Sedated urinary catheter placement was performed using midazolam (0.25 mg/kg IV), ketamine (3.5 mg/kg IV) and propofol (4 mg/kg IV) titrated to effect. An 11 cm urinary catheter (Tomcat Urethral Catheter; Smiths Medical ASD) was placed with mild resistance using the standard technique.¹⁴ A catheterized urine sample was submitted for urinalysis and culture (Table 2). Abdominal radiographs revealed possible mild peritoneal effusion (see Figure A in the supplementary material). After 12 h, the intravenous (IV) fluid rate was decreased to 3 ml/kg/h, which was continued until discharge. The cat was hospitalized for 41 h and received supportive therapy and monitoring consistent with patient needs. The cat urinated after urinary catheter removal, was administered robenacoxib (2 mg/kg SC) and discharged home with buprenorphine (0.01 mg/kg transmucosally q8h), gabapentin (10 mg/kg PO q8h) and prazosin (0.5 mg PO q12h).

After discharge, the cat was anorexic and lethargic but urinating normally. At 36 h after discharge, the cat became profoundly lethargic and passed severely hemorrhagic urine with large blood clots, without signs of stranguria or pollakiuria. The cat was presented to the emergency room 55 h after discharge. On examination, the cat was afebrile but tachycardic (heart rate 280 bpm), with weak femoral pulse quality, 5% dehydration, ptyalism and a mildly distended, painful abdomen. The urinary bladder was small on palpation. Blood pressure was initially too low to obtain a reading, and electrocardiography showed sinus tachycardia. A bolus of Normosol-R (10 ml/kg IV) was administered over 15 mins, resolving the hypotension. Point-of-care ultrasound revealed effusion in the hepatorenal, splenorenal and cystocolic quadrants, along with a small urinary bladder containing a large, mobile, gravity-dependent hyperechoic structure consistent with a blood clot. In-house bloodwork (Table 1) and diagnostic ultrasound-guided abdominocentesis were performed. The abdominal fluid was serosanguinous, with a fluid: blood potassium ratio of 2.0, consistent with a diagnosis of uroperitoneum.¹

The patient was hospitalized and administered maropitant (1 mg/kg IV) and Normosol-R (3 ml/kg/h IV). Urinary catheter placement was performed under sedation using midazolam (0.25 mg/kg), ketamine (2 mg/kg) and alfaxalone (2 mg/kg) titrated to effect IV. An 11 cm urinary catheter (Tomcat Urethral Catheter; Smiths Medical ASD) was passed with mild resistance that resolved with retropulsion. A catheterized urine sample was submitted for urinalysis and culture (Table 2). A right lateral radiograph was performed (Figure 1). In hospital, the cat received ampicillin-sulbactam (40 mg/kg IV q8h), enrofloxacin (5 mg/kg IV q24h), methadone (0.15 mg/kg IV q6h) and ketamine constant rate infusion (CRI; 0.1 mg/kg/h).

Figure 1

Right lateral abdominal radiograph after urinary catheter placement during second hospitalization for uroabdomen. Retroperitoneal effusion, peritoneal effusion and appropriate urinary catheter placement are evident

On reassessment the next morning, the cat was obtunded, 5–7% dehydrated and anuric with moderate abdominal pain and nausea; blood clots were visible in the proximal urinary catheter collection system. Point-of-care ultrasound revealed an empty bladder with subjectively more abdominal effusion in all quadrants of the abdomen. Bloodwork was rechecked (Table 1). Normosol-R was increased to 8 ml/kg/h, and fentanyl (3 µg/kg IV followed by a CRI at 3 µg/kg/h) and ondansetron (0.3 mg/kg IV q8h) were administered in addition to previous analgesic and anti-nausea medication. Focal urinary ultrasound was performed by a board-certified radiologist (Figure 2; see also Figure B in the supplementary material).

Figure 2

Ultrasound images of the urinary tract on day 2 of the second hospitalization for uroabdomen. (a) Longitudinal image of the left kidney, demonstrating renomegaly, medullary rim sign, surrounding perinephric steatitis and retroperitoneal effusion. (b) Longitudinal image of the left kidney, demonstrating moderate dilation of the renal pelvis. (c) Longitudinal image of the left kidney, demonstrating mild proximal hydroureter. (d) Longitudinal image of the right kidney, showing an avascular anechoic structure containing hyperechoic material present in the cranial cortex; the right kidney is enlarged, and there is surrounding perinephric steatitis, retroperitoneal effusion and a medullary rim sign. (e) Longitudinal image of the right kidney, demonstrating that the anechoic structure in the cranial cortex is avascular. (f) Transverse image of the right kidney, showing the cranial avascular anechoic structure and mild proximal hydroureter. Severe urinary cystitis and peritoneal effusion were also present, but not displayed in this figure (refer to Figure B in the supplementary material for the ultrasound report)

Due to progressive abdominal pain and effusion, mild hyperkalemia (serum potassium 6.08 mmol/l) (Table 1) and anuria, the patient underwent general anesthesia for a fluoroscopic retrograde positive contrast cystourethrogram via previously described methodology.¹⁵ Before the anesthesia, regular insulin (0.5 U/kg IV) and dextrose 50% (1 ml/kg IV) diluted 1:1 were administered for hyperkalemia. Fentanyl (3 µg/kg IV) and midazolam (0.3 mg/kg IV) were administered, followed by induction with alfaxalone (1 mg/kg IV) and maintenance with isoflurane, fentanyl (3 µg/kg/h) and ketamine (0.3 mg/kg/h). Normosol-R (4 ml/kg/h) was administered during the procedure. The cystourethrogram did not reveal evidence of bladder or urethral rupture (Figure 3); therefore, an exploratory laparotomy was pursued to identify the cause of the uroperitoneum.

Figure 3

Positive contrast cystourethrogram performed on day 2 of the second hospitalization for uroabdomen. A lateral caudal abdominal fluoroscopic image is presented, which demonstrates no leakage of contrast material from the bladder or urethra. Note that contrast material did leak antegrade out of the external urethral orifice as it was not clamped during the procedure. Incomplete distension of the bladder occurred despite incremental instillation of 13 ml/kg of diluted iohexol contrast material, which was noted to reflux into the ureters, renal pelvis and renal diverticulum bilaterally. The cranial aspect of the kidneys were not visible in the views obtained in the study

Cefazolin (22 mg/kg IV q1.5h) was administered intraoperatively. After routine aseptic preparation, a standard ventral midline laparotomy was performed. No urine leakage was observed from the bladder or abdominal urethra. Bilateral renomegaly was noted, along with significant retroperitoneal hemorrhage (Figure 4) and uroretroperitoneum (retroperitoneal fluid:blood creatinine ratio 3:1, retroperitoneal fluid:blood potassium ratio 2:0). Urine leakage was observed from both renal pelvises and the left renal parenchyma.

Figure 4

Intraoperative and post-mortem images of the urinary tract. (a) Left and (b) right renomegaly with significant retroperitoneal hemorrhage and uroretroperitoneum. (c) The bladder wall was severely thickened with a small omental adhesion at the apex of the bladder (transected with electrocautery before photograph). Intraoperatively, a sterile urinary catheter was placed retrograde from the urethra to fill the bladder with sterile saline. No leaks were identified from the bladder or abdominal urethra. (d) The entire urinary tract was removed post mortem. Renomegaly, subcapsular bruising, parenchymal hemorrhage and sloughing of the renal capsule and parenchyma were noted, consistent with tissue necrosis. The proximal half of the right ureter was small and dark compared with the left ureter. (e) Post-mortem examination of the left kidney demonstrated sloughing of the dorsolateral renal capsule, with urine leakage confirmed intraoperatively from this site as well as the left renal pelvis. (f) The right kidney showed similar subcapsular bruising without evidence of capsular sloughing. Urine leakage was identified from the right renal pelvis

Progressive hypotension occurred intraoperatively. Norepinephrine (0.1 µg/kg/min) was initiated and inhalant anesthesia was discontinued. Total intravenous anesthesia was maintained with fentanyl, ketamine and midazolam (0.2 mg/kg/h) CRIs. Left ureteronephrectomy and right subcutaneous ureteral bypass placement was offered as a salvage procedure; however, euthanasia was elected intraoperatively because of a poor prognosis. Post mortem, the entire urinary tract was removed (Figure 4) and submitted for histopathology (Figure 5; see also Figure C in the supplementary material). Aerobic and anaerobic cultures of the renal pelvis and parenchyma yielded no growth.

Figure 5

Histopathologic images of the urinary tract post mortem. Within the medullary interstitium of both kidneys, moderate numbers of neutrophils were present, most prominent the renal pelvis, with extension deeper into the medullary interstitium in one kidney. Both kidneys also revealed marked dilation and expansion of the renal pelvis by acute hemorrhage and fibrin. Hemorrhage and fibrin extended into the medullary and cortical interstitium, communicating through to the renal capsule, which was also distended by hemorrhage and fibrin. The pelvic uroepithelium was multifocally ulcerated and replaced by acute hemorrhage and fibrin in both kidneys. Occasionally, renal medullary tubules contained proteinaceous casts and rare intratubular erythrocytes. Moderate ureteral dilation and periureteral steatitis with hemorrhage were noted. The urinary bladder showed moderate to marked mucosal expansion due to edema, along with a small amount of acute hemorrhage. Occasional ulceration of the mucosal epithelium in the urinary bladder was observed, as well as replacement by fibrin and hemorrhage. Low numbers of lymphocytes and plasma cells were present within the bladder mucosa. (a,b) H&E, × 0.6 magnification, low magnification photomicrographs of both kidneys, showing marked pelvic dilation, pelvic hemorrhage and subcapsular hemorrhage. (c) H&E, × 0.8 magnification, photomicrograph of the kidney showing hemorrhage extending from the pelvis through the cortex and communicating with subcapsular space. (d) H&E, × 11.4 magnification, photomicrograph of the kidney showing disruption of the ureothelium at the pelvis and infiltrating neutrophils, hemorrhage and fibrin into the adjacent medulla. (e) H&E, × 16.0 magnification, photomicrograph of the kidney at the level of the medullary and cortical interface with infiltrating neutrophils in the medullary interstitium extending slightly into the cortex. (f) H&E, × 7.0 magnification, photomicrograph of the ureter with surrounding inflammation and hemorrhage in the periureteral adipose tissue. (g) H&E, × 1.0 magnification, photomicrograph of the urinary bladder showing marked expansion of the mucosa by edema and moderate hemorrhage. (h) H&E, × 6.7 magnification, high-magnification photomicrograph of the ulcerated urothelium with replacement by hemorrhage and fibrin, with mild to moderate cystitis. H&E = hematoxylin and eosin

Discussion

This case report describes an unreported and irreparable cause of uroabdomen in a cat. It is suspected that renal hemorrhage led to bilateral ureteral obstruction, renal pelvic and parenchymal rupture, and ultimately, uroabdomen. The underlying cause of severe renal hemorrhage remains unknown. The cat initially experienced recurrent lower urinary tract signs and feline idiopathic cystitis was suspected; however, renal hematuria resulting in secondary UO was possible given the progression of this case. The administration of prazosin may have contributed to recurrent lower urinary tract signs, as its usage has been recently questioned as a result of unproven benefit^16,17 and increased risk of recurrent UO.¹⁸ Nonetheless, before the second hospitalization, the cat passed profusely hemorrhagic urine and did not have clinical findings consistent with UO.

Upper urinary tract sources of hematuria are uncommon in cats, and occur with acute tubular necrosis, pyelonephritis, coagulopathies, glomerular disease, idiopathic renal hematuria, nephrolithiasis, neoplasia, trauma and renovascular disorders.¹⁹ Coagulopathy cannot be definitively excluded in this case, as coagulation testing was not performed. The cat was thrombocytopenic based on the in-house complete blood count (CBC); however, studies have demonstrated poor correlation between automated and manual platelet counts in cats.^20,21 Moreover, the cat had a normal manual platelet count during its first assessment for lower urinary tract signs on day –12 (Table 1), did not have access to rodenticide and had no extraurinary signs of hemorrhage, making a coagulopathy unlikely. In addition, spontaneous hemorrhage due to primary thrombocytopenia typically occurs with platelet counts less than 30–35 K/µl.^22,23 Renal ischemia was also not definitively ruled out as renal blood flow was not assessed using ultrasonography; however, no additional evidence of pathologic thrombosis was identified clinically or during surgical exploration, the renal pathology was bilateral and histopathologic findings were not consistent with ischemia.²⁴

Severe idiopathic renal hematuria was strongly considered as a differential diagnosis in this case; however, it remains a diagnosis of exclusion. Although it is a rare cause of acute, intermittent or chronic gross hematuria and has been sporadically reported in dogs,^25–33 reports in cats are limited.³⁴ Because of its small internal diameter (0.4 mm), the feline ureter is highly susceptible to obstruction.^35,36 Lower urinary tract signs can occur in up to 25% of cats with ureteral obstruction.³⁶ In this case, there was no definitive evidence for an obstructive uropathy during the cat’s second hospitalization; however, ultrasonography is variably accurate in diagnosing ureteral obstruction.^37,38 Furthermore, the renal pelvic and ureteral diameters were likely underestimated because of rupture. In humans, renal pelvic rupture can result from increased renal pelvic pressure from ureteral obstruction,^7,9,10 with a similar case reported in a cat.¹¹ In dogs, the lateral aspect of the renal capsule appears to be the weakest region,³⁹ and it is likely that intrarenal pathology in this case led to weakness, resulting in parenchymal rupture.

It remains unclear whether renal hemorrhage or pyelonephritis was the primary pathologic process in this case. Histopathology confirmed moderate neutrophilic inflammation consistent with pyelonephritis, though it was most likely sterile, as no infectious agents were identified on urinalysis, culture or histopathology. However, a definitive diagnosis of bacterial pyelonephritis remains difficult.⁴⁰ It is unlikely that pyelonephritis resulted from prior UO, as this typically results in lymphoplasmacytic inflammation, and the severity of bladder and renal lesions often parallels the degree of hyperkalemia,⁴¹ which was absent at time of UO. Although such extensive hemorrhage is not typical of pyelonephritis,^42,43 acute inflammation may have led to vascular damage and subsequent hemorrhage, particularly as trauma and coagulopathy were unlikely contributors. However, given the moderate degree of pyelonephritis but extensive renal hemorrhage, it is possible that pyelonephritis developed secondary to tissue injury from hemorrhage.⁴⁴ The underlying cause of the hemorrhage remains undetermined. No developmental vascular anomalies were evident; however, given the cat’s young age, an undiagnosed vascular disorder is possible, but difficult to prove.

Regarding the case management of uroabdomen, antimicrobials are generally reserved for cases with confirmed urinary tract infection and urosepsis; they are sometimes used empirically in high-risk cases.¹ Broad-spectrum antibiotics were commenced in this case, as the cat presented in a critical condition, iatrogenic urinary tract infection was possible given recent urethral catheterization,^45,46 urinalysis results were not readily available and in-house automated CBC revealed leukocytosis. Although cefazolin is often used for peri-procedural prophylaxis,⁴⁰ the cat was already receiving ampicillin-sulbactam, raising concerns about antibiotic resistance due to this de-escalation and overlapping coverage approach. The selection of antimicrobials likely represents a case management flaw, given the apparently sterile nature of the uroabdomen.

The positive contrast cystourethrogram did not include a complete view of the kidneys, as it is typically performed to diagnose bladder or urethral tears.¹ If reflux into the ureters occur, a complete view of both kidneys may allow diagnosis, as renal rupture may provide a path of decreased resistance. In this case, abdominal ultrasound could have been performed during the first hospitalization, as a result of subtle abnormalities on the cat’s abdominal radiographs, potentially allowing earlier identification of abnormal renal parenchyma and early retroperitoneal or peritoneal effusion. It is unclear what significance this may have had on the management and outcome of this case, as 59.8% of cats with UO have pericystic effusion and 35.6% have retroperitoneal effusion.⁴⁷ Other diagnostics, including coagulation testing, CT or exploratory laparotomy, may have helpful if performed earlier in this case.

Conclusions

This case report describes a novel cause of uroabdomen resulting from renal hemorrhage and pyelonephritis with secondary renal rupture. Atraumatic renal pelvic and parenchymal rupture should be considered a differential diagnosis for uroabdomen, and more specifically, uroretroperitoneum. The underlying cause of severe renal hemorrhage in this cat remains unknown.

Supplemental Material

Supplementary figure A

Abdominal radiograph radiology report from the patient’s first hospitalization (day 0).

Supplemental Material

Supplementary figure B

Focal urinary ultrasound radiology report from the patient’s second hospitalization (day 2.5).

Supplemental Material

Supplementary figure C

Histopathology report for the urinary tract submitted postmortem.

Footnotes

Acknowledgements

The authors would like to acknowledge the technicians, doctors and support staff that were involved in the care of this patient. In addition, the authors would like to acknowledge the pet parents of this patient, as they were extremely dedicated and provided him with the highest level of love and care.

Accepted: 11 March 2025

Supplementary material

The following files are available as supplementary material:

Supplementary figure A: Abdominal radiograph radiology report from the patient’s first hospitalization (day 0).

Supplementary figure B: Focal urinary ultrasound radiology report from the patient’s second hospitalization (day 2.5).

Supplementary figure C: Histopathology report for the urinary tract submitted postmortem.

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

The work described in this manuscript involved the use of non-experimental (owned or unowned) animals. Established internationally recognized high standards (‘best practice’) of veterinary clinical care for the individual patient were always followed and/or this work involved the use of cadavers. Ethical approval from a committee was therefore not specifically required for publication in JFMS Open Reports. Although not required, where ethical approval was still obtained, it is stated in the manuscript.

Informed consent

Informed consent (verbal or written) was obtained from the owner or legal custodian of all animal(s) described in this work (experimental or non-experimental animals, including cadavers, tissues and samples) for all procedure(s) undertaken (prospective or retrospective studies). No animals or people are identifiable within this publication, and therefore additional informed consent for publication was not required.

ORCID iD

Amanda M Spillane

Marie T Keith

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