An unusual case of a traumatic splenic rupture masquerading as myocardial ischemia: A case report

DOI: https://doi.org/10.21203/rs.3.rs-1516876/v1

Abstract

Background

Spleen is one of the frequently injured abdominal organs during trauma which could result in intraperitoneal bleeding of life-threatening magnitude. Even though, splenic injury ensuing trivial trauma accounts for a minor fraction of splenic injury and might go unnoticed, delayed or missed diagnosis and management could result in a complicated clinical course.

Case Description

One such event is presented here, wherein late diagnosis of an advanced grade splenic injury following a trivial trauma initially presented in disguise as acute myocardial ischemia in a previously healthy South Asian lady in her late 30s. Emergency laparotomy and splenectomy were performed with simultaneous massive transfusion for a 3.5-liter blood loss. She had an uncomplicated clinical course with regular surgical follow-up.  

Conclusion

Splenic injuries might present with atypical symptoms such as uncharacteristic chest pain and shoulder pain, necessitating attending clinicians to have a high degree of suspicion especially in busy units such as the emergency department.

Background

Traumatic splenic rupture is seen in around 32% of blunt injuries to the abdomen, predominantly following road traffic accidents and falls [1]. Initial presentation following a splenic injury varies from mild left hypochondriac pain, radiating pain to the left shoulder [2], or hemodynamic instability depending on the degree of blood loss. In hypovolaemic patients, anaemia and hypoxia might lead to myocardial ischaemia following advanced grades of splenic injuries. Clinically sinister splenic injuries following relatively minor injuries should be given closer attention as there could be predisposing microscopic and macroscopic anomalies in the spleen. Herein, we present a unique case of a splenic injury following a minor trauma initially presented with atypical chest and radiating pain to left shoulder with haemodynamic stability. Initial failure to elucidate the trauma and presence of electrocardiogram (ECG) features suggestive of inferior ischaemia during the first medical contact resulted in management of the episode in the line of myocardial ischemia with antiplatelets and anticoagulants. This case report highlights the necessity of exclusion of more sinister differential diagnoses such as underlying splenic injuries in cases of combination of symptoms of atypical chest and shoulder pain which might lead to considerable modifications in subsequent management and resultant favourable outcomes.

Case Description

A 39-year-old American society of Anaesthesiology stage 1, body mass index 23 kgm− 2, South Asian female presented to the emergency department (ED) of a District General Hospital in Sri Lanka with atypical chest pain and left shoulder pain for three days’ duration. She did not disclose any autonomic features, difficulty in breathing, or cough with fever. On examination, she was not pale. Her cardiorespiratory parameters were stable (Non-invasive blood pressure 112/67mmHg, pulse rate 88 per minute, peripheral oxygen saturation, 98% on room air and respiratory rate, 16 per minute). She denied any history of trauma. There was no localized tenderness over the chest. The COVID-19 rapid antigen test was negative. The ECG showed ‘T’ inversions in inferior leads (lead II, II and aVF). Troponin I titer was negative. Chest X-ray was normal. She was diagnosed as having unstable angina considering her persistent symptoms. Loading doses of oral aspirin 300 mg, clopidogrel 300 mg, and atorvastatin 40 mg were prescribed with 60 mg subcutaneous enoxaparin twice a day. Subsequently, she was transferred to the medical unit. The repeated ECG did not reveal any dynamic changes. During the ward stay, she complained of persistent symptoms for which sublingual glyceryl trinitrate was administered. Rest of the blood investigations yielded normal results. Eighteen hours after admission, a sudden haemodynamic collapse was witnessed. Her blood pressure dropped to 70/40mmHg and pulse rate increased to 120 per minute with very low volume. She was found to be severely pale. The repeated haemoglobin level was 3.8 g/dl. Immediate resuscitation was commenced with supplemental oxygen. Massive transfusion protocol with transfusion of blood and blood products was initiated. Further history revealed that the patient had an accidental fall onto a hard surface from an approximate height of 2 feet with impact on her left loin around the time of onset of the presenting symptoms. An ultrasound scan of the abdomen revealed a splenic laceration with expanding subscapular haematoma and haemoperitoneum. Following heamatology opinion, intravenous Tranexamic acid 10 mg/ kg and Protamine sulfate 1mg/ kg was administered. Details of the results of the initial and subsequent investigations are illustrated in Table 01.

She was taken to the operating theater for emergency exploratory laparotomy. On induction, her blood pressure was 92/65mmHg and her pulse rate was 100 per minute. She was induced with intravenous ketamine 50 mg, midazolam 1 mg, and fentanyl 75 mics. During the surgery, two linear lacerations extending from the capsule to the hilum were detected in the mid part of the spleen with a large haematoma accountable for the American Association for the Surgery of Trauma (AAST) grade 4 splenic injury with an estimated progressive blood loss of 3.5L which warranted urgent splenectomy with ongoing massive blood transfusion. Spleen was found to be congested with an approximate size was 10 cm* 6 cm * 5 cm (Fig. 1a, b).

Massive transfusion was continued requiring 6 units of packed red cells, 600 ml of fresh frozen plasma, 20 units of cryoprecipitate, and an adult pool of platelets. Splenectomy was performed by the surgical team. There was no other visceral organ injury. Haemostasis was achieved and the patient was admitted to the intensive care unit. Clotting parameters were assessed by way of prothrombin time, activated partial thromboplastin time, and platelet count due to the unavailability of point of care testing. All yielded normal results. Ten hours later, with stable haemodynamics and normalized arterial blood gas analysis, the trachea was extubated. Her ECG changes reverted back to normal within 24 hours. On postoperative day two, she was transferred back to the ward. 2d echocardiogram did not reveal regional wall motion abnormalities. A coronary angiogram was arranged on outpatient basis after 2 weeks, which revealed normal coronary vasculature. Lipid profile and fasting blood sugar level were normal. Spleen weighed 150 g which was normal for age and sex. Histology of the spleen did not reveal chronic abnormalities (Fig. 2a, b).

The patient was regularly followed up in the surgical clinic, with pneumococcal, meningococcal, and haemophilus influenzae b vaccinations arranged at 2 weeks. At one-year follow-up, she had been devoid of any life-threatening sepsis or any other surgery-related complications. Screening for Epstein-Barr virus, Cytomegalovirus, Human immunodeficiency virus, Hepatitis A/B/C, and malaria were negative. Following the incident, ED doctors were briefed on the sequence of events. The necessity of complete history, examination with increased vigilance on trauma were reiterated and the exclusion of probable differential diagnoses by relevant history, clinical examination and utility of subsidiary investigations such as bedside FAST, whenever appropriate, was encouraged especially in presentations with atypical chest pain.

Discussion

Spleen, the largest organ in the lymphatic system, lies between the 9th and 11th ribs in the left hypochondriac region [3]. It is considered the most frequently damaged organ following blunt trauma to the abdomen [4]. Its soft consistency, sinusoidal structure, fragile capsule, and highly vascular nature make it more prone to injury with the potential for life-threatening internal haemorrhage [5].

Patients may present with varying degrees of symptomatology following splenic injury. Left hypochondriac and pleuritic type chest pain are common [6] while a referred type left shoulder pain is found in around 20% of patients called the Kehr sign [2]. Features of peritonitis and hypovolaemia may be evident in patients with internal bleeding. Focussed assessment of sonography of trauma (FAST) might reveal splenic injury with intraperitoneal bleeding. Computed tomography (CT) is considered the gold standard imaging modality with increased sensitivity and specificity. Further, it aids in staging the severity of the injury which might direct the management in either operative or non-operative pathway [7]. ECG changes associated with splenic injury could be resultant of multiple factors. Hypovolaemia and tachycardia leading to impaired myocardial perfusion/demand balance and associated myocardial contusions, especially in the background of concurrent chest injuries could result in varying degrees of such changes [8]. It is imperative to resuscitate without delay and look for chest injuries in such instances.

In literature, anticoagulants and antiplatelets have been implicated as causative factors of atraumatic splenic rupture [912]. Further, the outcome following splenic trauma in patients who were already on anticoagulants was found to be worse in a study by Bhattacharya et al [13]. By careful analysis of the sequence of events in our case, it is possible that the patient acquired a minor degree of splenic injury during the trauma and the grade of injury was advanced by concurrent therapy with dual antiplatelets and low molecular weight heparin due to clot dislodgment or reactionary haemorrhage. The possible mechanism of her initial ECG is unclear as she was haemodynamically stable on presentation and subsequent cardiac assessment was normal. We came across a very similar case of a ruptured spleen needing exploratory laparotomy reported by Allan et al, 20 years ago [14]. The authors came across similar ECG changes in an elderly patient with known coronary artery disease initially presented with ischemic type chest pain, subsequently managed as unstable angina with IV heparin. Persistent haemodynamic instability despite fluid therapy and worsening left hypochondriac pain warranted a CT scan of the abdomen which revealed features suggestive of splenic injury and gross haemoperitoneum, necessitating urgent laparotomy. Akin to our case, there had been a trivial injury not disclosed during the initial medical assessment.

Had the patient disclosed the trauma, there was a chance of detection of lower grade splenic injury and avoidance of antiplatelet and anticoagulant therapy. Despite the unavailability in our center, transferring her to the nearby tertiary care center for CT scan with contrast studies, considering her initial haemodynamic stability was a possibility to further delineate the degree of splenic injury. Non-operative management could have been attempted depending on sustained haemodynamic stability and CT findings. Whether there was a delayed rupture of the spleen precipitated by medical therapy could not be elucidated due to the unavailability of advanced histological studies and staining techniques in our institution.

The patient presented to our institution around the first wave of the COVID-19 pandemic in Sri Lanka where perceived fear of acquiring the infection was noticeable among the public. The effects of COVID-19 on health care seeking behaviour, misdiagnosis due to strayed focus from COVID-19 non-related conditions, indirect contact resultant of telecommunication and use of personal protective equipment (PPE) and strain on health care workers had already been discussed in the literature [15] which may have been contributory factors in this clinical scenario. It is thus imperative to encourage patients to disclose relevant details pertaining to their presentation. In-depth situational analysis in cases of misdiagnosis or treatment, creating a feedback system enforcing the correct decision-making process, and setting up local guidelines are pivotal in such cases.

Conclusion

Blunt abdominal trauma may present initially with ambiguous clinical signs overlooking any serious internal abdominal injury, making assessment more challenging. Exercising high degree of suspicion may be the only key to set the right trajectory of clinical management. Splenic injury is notorious to cause detrimental clinical outcome when misdiagnosed, where high grade injury is ensued secondary to trauma, as in the illustrated case, could also follow the same downward spiral into a debacle if not intervened in a timely manner. It cannot be overemphasized the importance of guided physical examination and bed side testing such as FAST to delineate the working diagnosis specially in ED setup to avoid astray in erroneous management pathways.

Abbreviations

electrocardiogram: ECG

emergency department: ED

American Association for the Surgery of Trauma (AAST)

Focussed assessment of sonography of trauma: FAST

Computed tomography: CT

Declarations

Ethics approval and consent to participate: Ethical approval was not required for preparation of the manuscript as all identifiable patient details were nullified. 

Consent for publication: Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal

Availability of data and materials: Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Competing interests: No financial or non-financial competing interests are declared by the authors.

Funding: No external funding was received.

Authors' contributions:

BM managed the patient, conceived the idea for the manuscript, obtained consent, collected data and conducted the literature review and wrote the initial version of the manuscript.

UPM managed the patient and contributed to compilation of the manuscript.

TK managed the patient and contributed by providing images and conducting literature review.

All authors approved the final manuscript.

Acknowledgements

The authors would like to acknowledge Dr. K.D.T. Dilrukshi (Consultant Physician) and Dr. N.D. Ranatunga (Consultant Pathologist) of our institution for contributing during patient management and provision of histological reports, respectively.

References

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Table 1

Table 1. Preoperative Investigation results      

Investigation

Value

Reference

 

On admission

Immediately following haemodynamic collapse

 

White blood count

10200

13,000

4-11,000/mm3

Haemoglobin

13.6 

3.8

10-14 g/dl

Haematocrit

40.2%

13.1

35-55%

Platelets

254,000

120,000

150-450,000/mm3

Serum Na+

145 

142

135-155 meq/l

Serum K+

4.4 

4.1

3.5-5.5 meq/l

Blood urea

3.9 

4.3

3.3 -6.6 mmol/l

Serum Creatinine

0.8 

0.9

0.7-1.3 mg/ dl

Aspartate aminotransferase

25 

36

10-35 u/l

Alanine aminotransferase

28 

40

9- 55 u/l

Prothrombin time

10 

20

11-13 seconds

INR

0.9

1.58

0.8- 1.1

Activated partial thromboplastin time

33 

64

30- 40 seconds

Serum Amylase

50 

55

40- 140 u/l

Serum Bilirubin

0.9

1.0

< 1.2 mg/ dl

Arterial blood gas analysis

Not performed

pH           7.20

PCO2       36

PO2         250(O2 15l/min)

 

HCO3-     16

Base excess- -10

Lactate     6.6 

7.35-7.45

35-45mmHg

80-100mmHg (room air)

 

22-26 meq/l

-2- +2

<2mmol/l