Point of Care Ultrasound Utility in the Setting of Chest Pain: A Case of Takotsubo Cardiomyopathy
Department of Medicine, University of Arizona - Tucson and Banner University Medical Center, Tucson
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Department of Medicine, University of Arizona - Tucson and Banner University Medical Center, Tucson
Andrew Kim DO
Cristian Valdez DO
Tony Alarcon MD
Elizabeth Benge MD
Blerina Asllanaj MD
MountainView Hospital
Las Vegas, NV USA
Abstract
This is a report of a 27-year-old male with known history of Addison’s disease, noncompliant with medications, and hypothyroidism who presented with shortness of breath, nausea, vomiting, fever, and chest pain as well as Brugada sign seen on electrocardiogram. Echocardiogram revealed a moderate pericardial effusion and laboratory findings were suggestive of adrenal insufficiency. Patient was determined to have Type I Brugada phenocopy, which is a Brugada sign seen on EKG with a reversible cause. In this instance, the Brugada phenocopy was caused by adrenal insufficiency with associated pericarditis. Treatment with high-dose steroids led to resolution of both the pericardial effusion and Brugada sign, providing further evidence of Brugada phenocopy.
Keywords: Brugada Phenocopy, Adrenal insufficiency, Pericarditis, Brugada Sign
Case Presentation
History of Present Illness
A 27-year-old man was admitted for left-sided chest pain. Electrocardiogram (EKG) taken in the emergency department showed suspicious Brugada’s sign in leads V2 and V3 (Figure 1).
Figure 1. Initial EKG showing rhythm with signs of inferior infarct based on findings of leads II, II aVL. There are also signs of anterolateral injury seen in leads V2-V5. Also, there were coved ST elevation in leads V2 and V3, suggesting a Type I Brugada sign. (Click here to open Figure 1 in an enlarged, separate window)
He had been feeling short of breath, nauseous, had multiple episodes of vomiting without blood, fever of up to 102 F, and chills for five days prior to admission that had resolved. He described the pain as similar to a “pulled muscle” over his left pectoral area that was worse with extension of the left shoulder as well as with deep inhalation. He denied palpitations, diaphoresis, or radiation of the pain. He denied any family history of cardiac disease or sudden cardiac deaths. Patient lives in San Francisco and travels to Las Vegas periodically to see his family. He had been in Las Vegas for four months prior to admission. He works as a video editor from home. He denies intravenous drug use, history of sexually transmitted illnesses, or history of unsafe sexual activity.
Upon admission, his vitals were: Temp 36.2° C, BP 97/66, HR 84, respiratory rate 16, and SpO2 94% on room air. The patient was slightly hyponatremic with sodium level 131. Potassium levels were also low at 3.2. Physical exam was unremarkable with benign cardiac and respiratory findings. Chest X-ray showed small left-sided pleural effusion with surrounding area of atelectasis. The right lung was unremarkable. In light of the patient’s symptoms and abnormal EKG, an echocardiogram was planned to assess cardiac function and further lab studies were ordered.
Past Medical History
The patient was diagnosed with Addison’s disease at a young age and started on hydrocortisone 5mg daily. Patient also has a history of hypothyroidism and takes levothyroxine 50 mcg daily. Patient has a history of psoriatic arthritis and was taking methotrexate before switching to injectables. Of note, the patient states that he is noncompliant with his oral hydrocortisone 5 mg, sometimes missing multiple days at a time. He had missed three to four days of medication before symptom onset, and had been taking stress doses of 20 mg a day for five days. Given the patient’s presentation and reproducible pain with movement of the left arm, initial differentials included left pectoral strain and community acquired pneumonia. Adrenal insufficiency and autoimmune pericarditis were also considered based on the patient’s history of autoimmune disorders.
Investigation
On day two of hospitalization, the patient continued to be hypotensive and febrile. Cortisol levels were found to be 1.02 mcg/dL, adrenocorticotropic hormone (ACTH) less than 1.5 ug/mL, TSH was 1.65 mcg/mL and T4 was 1.67 ng/dL. Urinalysis showed protein, a small amount of ketones, blood, nitrites, 0-2 red blood cells, 10-20 white blood cells, and 5-10 epithelial cells but was negative for leukocyte esterase and bacteria. Inpatient echocardiogram done on day two of hospitalization demonstrated a small to moderate pericardial effusion that appears complex with possible calcifications of visceral pericardium at the right ventricular apex (Figure 2).
Figure 2. Echocardiogram. A: shows a pericardial effusion lateral to the left atrium, 1.20 centimeters in diameter. B: shows a pericardial effusion at the apex of the right ventricle, 1.24 centimeters in diameter. (Click here to open Figure 2 in an enlarged, separate window)
Immunologic work-up was also completed and demonstrated high complement C3 at 187 mg/dL. Viral work-up was also negative. Further investigation of history revealed that the patient had experienced similar symptoms in the past - shortness of breath, fever, nausea - especially during stressful times in his life, but attributed it to anxiety.
Management
Patient was immediately started on intravenous hydrocortisone 50mg every 6 hours after cortisol labs were returned, with the plan to wean to twice a day on the next day and then switching to oral hydrocortisone 20 mg daily. The patient was also started on ceftriaxone 1 gram daily for possible urinary tract infection and doxycycline 100mg twice a day. He complained of dizziness and weakness after switching to oral hydrocortisone, and the dosage was increased to 25 mg daily. The patient stated that after the increase in steroids these symptoms resolved and he had increased energy. His blood pressure remained stable with no episodes of hypotension after switching to oral steroids and his electrolyte panel remained within normal limits.
Follow-up echocardiogram on day five of hospital stay demonstrated a trivial pericardial effusion that had decreased significantly in comparison to the previous study (Figure 3). Repeat electrocardiogram demonstrated normal sinus rhythm with no Brugada sign (Figure 4).
Figure 3. Slight pericardial effusion lateral to the right ventricle, 0.6 centimeters in diameter. Note that there is marked decrease in fluid along the left atrium and apex of the right ventricle compared to Figure 2. (Click here to open Figure 3 in an enlarged, separate window)
Figure 4. Electrocardiogram taken after steroid treatment prior to discharge. Normal sinus rhythm seen in results. Also note normalization in leads V2 and V3 with no clear Brugada seen. (Click here to open Figure 4 in an enlarged, separate window)
Discussion
Our patient’s presentation of shortness of breath, nausea, vomiting, fever, and chest pain with negative viral work-up is suggestive of early stages of adrenal insufficiency crisis. Our diagnosis is further evidenced by the patient’s noncompliance with his home steroid doses as well as a morning cortisol level of 1.02 mcg/dL and ACTH less than 1.5 ug/mL. There have been reported cases of adrenal insufficiency causing Type I Brugada phenocopy and normalization with treatment (1). The normalization of our patient’s EKG and pericarditis after treatment with high dose steroids is evidence of Brugada phenocopy in this case. In addition, pericarditis has been shown to present as a Type 1 Brugada phenocopy (BrP), a Brugada sign seen on EKG with a reversible cause (2).
One common cause of BrP is electrolyte abnormalities, as BrP can be seen in patients with profound hyponatremia and hyperkalemia (3,4). In particular, hyperkalemia is a common culprit of Brugada sign on EKG as potassium excess can decrease the resting membrane potential (5). Typically, patients with adrenal insufficiency will exhibit electrolyte abnormalities that can explain Brugada sign on EKG. This patient’s electrolytes were indicative of hyponatremia and hypokalemia upon presentation. Although the electrolyte abnormalities were mild, the hyponatremia in particular contributed to the team’s initial suspicion of adrenal insufficiency. To our knowledge, this is the first instance of Brugada sign and pericarditis seen together in adrenal insufficiency crisis. Cases of Brugada pattern in adrenal crisis have been reported (6), however no echocardiogram was done in these case reports.
In addition, reported cases of pericarditis caused by Brugada phenocopy offers an alternative view of the sequence of events in this patient (7). Pericardial disease is known to cause Brugada phenocopy, and this may have been the case in our patient. Both pericarditis and BrP can be caused by adrenal insufficiency, so it is also possible that both of these events were independent of each other and stem from the underlying adrenal insufficiency. As such, this case highlights an important point mentioned in the previous case reports: the need to consider both pericarditis and adrenal insufficiency crisis in a patient presenting with Brugada phenocopy.
Conclusion
In conclusion, in patients presenting with Brugada sign the possibility of adrenal insufficiency crisis as well as pericarditis should be considered, especially in patients with known Addison’s disease. Furthermore, patients presenting with Brugada sign with no history of genetic cardiac history or family history of sudden cardiac death should be evaluated for other causes, such as adrenal insufficiency or pericarditis.
References
Cite as: Kim A, Valdez C, Alarcon T, Benge E, Asllanaj B. A Case of Brugada Phenocopy in Adrenal Insufficiency-Related Pericarditis. Southwest J Pulm Crit Care Sleep. 2022;25(2):25-29. doi: https://doi.org/10.13175/swjpccs033-22 PDF
Dr. Kriti Gupta, MD
Dr. Vipin K. Singh, MD
Dr. Zia Arshad, MD*
Dr. G. P. Singh, MD
*Corresponding Author
Department of Anaesthesiology
King George’s Medical University
Lucknow UP, India 226003
Abstract
Background: Delirium is common in critically ill intensive care unit (ICU) patients and has been documented in up to 87 percent of patients. Sleep deprivation and delirium have been associated. Alteration of melatonin production has been associated with delirium. Melatonin acts via melatonin receptors present in the suprachiasmatic nuclei (SCN) and promotes sleep by attenuating the wake-promoting signal from the SCN.
Objective: To determine the relationship between exogenous melatonin and the incidence of delirium and its association of with severity of illness, measured in term of APACHE II, procalcitonin level at the time of admission and daily SOFA score.
Patients and Methods:
Design: Randomised placebo-control study.
Setting: the study was conducted in critical care setting in a tertiary level ICU.
Participants: Postoperative patients age between 20-60 years who are going to be ventilated more than 48 hours without any contraindication to enteral medications.
Interventions: Study group received melatonin 5 mg through the enteral route.
Main outcome measures: To determine the effect of exogenous melatonin on the incidence of delirium in postoperative patients who require mechanical ventilation for more than 24 hours. The secondary outcome measures are procalcitonin (PCT) value at admission and disease severity scores like APACHE II and SOFA.
Results: No statistically significant difference was found in admission incidence of delirium or procalcitonin. Age was higher in those patients that developed delirium (p < 0.05).
Conclusions: Although the incidence of delirium is not affected by exogenous melatonin or higher APACHE scores, it had a significant correlation with higher procalcitonin, that in turn indicated an association with delirium and sepsis. It was found that there is increased risk of developing delirium with increasing age.
Key words: delirium, intensive care unit, sedation, melatonin, APACHE II, procalcitonin,
Introduction
Delirium is defined as “A disturbance in attention (i.e., reduced ability to direct, focus, sustain and shift attention) and awareness (reduced orientation to the environment)” (1). Delirium is extremely prevalent in hospitalized patients; it affects 10%–24% of the adult general medicine population and 37–46% of the general surgical population. Delirium has been documented in up to 87 percent of patients in the intensive care unit (ICU) (2). Multiple etiologies have been hypothesized to be causing delirium. Some of these are central cholinergic deficiency, reduced GABA activity, abnormal serotonin and melatonin pathways, cerebral hypo perfusion and neuronal damage due to inflammation (3,4). Acute Physiology and Chronic Health Evaluation II score (APACHE II) and the Sequential Organ Failure Score (SOFA) score have been found to aid in the prediction of delirium in the critically ill.
It has been demonstrated that pattern of secretion and concentration of melatonin are altered in critically ill patients (5). Melatonin release from the pineal gland is also decreased due to surgical stress and hence its potential use in postoperative delirium (6). Sepsis-associated delirium is a cerebral manifestation commonly occurring in patients with other infection-related organ dysfunctions and is caused by a combination of neuroinflammation and disturbances in cerebral perfusion (7). Procalcitonin is a helpful biomarker for early diagnosis of sepsis in critically ill patients (8).
Melatonin acts via melatonin receptors present in the suprachiasmatic nuclei (SCN) and promotes sleep by attenuating the wake-promoting signal from the SCN (9,10). Bioavailability of melatonin is excellent as demonstrated by supraphysiological level after exogenous supplementation (11).
The Confusion Assessment Method (CAM) is a diagnostic instrument used to screen and diagnose delirium in ICU. The CAM diagnostic algorithm is comprised of four components: (1) an acute (4) an altered level of consciousness. The diagnosis of delirium is based on the presence of both component 1 and 2, and either 3 and 4 (12).
Objective
The primary objective of the study was to determine the efficacy of exogenous melatonin in preventing delirium in postoperative patients admitted in ICU, as well as to compare the outcome by comparing the incidence of delirium and length of ICU stay in two groups. The secondary objective is to determine the association of delirium with severity of illness, which was measured in term of APACHE II and Procalcitonin level at the time of admission and daily SOFA scoring.
Methods
We performed a randomized, placebo-controlled study on postoperative patients admitted in our 20-bed tertiary level ICU. Inclusion criteria included adult postoperative patients requiring mechanical ventilation for more than 48 hours who were able to receive medication by the enteral route. Exclusion criteria included unwillingness to participate; sensitivity or history of allergic reaction to melatonin supplements; pregnancy; paralytic ileus; patients not expected to survive >48 hours; preexisting pathologies including cognitive dysfunction, dementia, psychiatric disorders or sleep disorders; history of head injury, substance abuse or withdrawal; and patients with hearing impairments.
Patients were randomized into two groups of 70 patients each with a sealed envelope randomization method. The study group received melatonin 5 mg via the enteral route at 8 pm every day and the control group received placebo (1 gm lactose powder) through a nasogastric tube until ICU discharge/transfer. APACHE II and procalcitonin (PCT) levels were recorded at admission, and SOFA scores were calculated daily. Delirium preventive measures including decreased light, noise, and regular patient orientation were applied uniformly in both groups. On the day of discharge/transfer the patients were evaluated using the CAM-ICU (Confusion Assessment Method) scale. The patients were categorized as “Delirious” or “Not Delirious” on the basis of the results from the CAM-ICU scale (12). Results were analyzed by comparing the incidence of delirium, length of ICU stay, APACHE II, SOFA Score and PCT value at the time of admission.
Results
A total of 140 adult post-operative patients transferred to the ICU who were ventilated more than 48 hours were evaluated. Table 1 contains the demographics of the study population.
Table 1: Between Group Comparison of Demographic Profile
Mean age of patients enrolled in the study was 38.70±11.56 years. Difference in age of patients in Group A (38.46±11.87) and Group B (38.94±11.33) was not statistically significant.
APACHE II scores did not differ at admission (Table 2).
Table 2: Between Group Comparison of APACHE II Score
Procalcitonin levels did not differ at admission (Table 3).
Table 3: Between Group Comparison of Procalcitonin (ng/ml)
Range of procalcitonin levels of patients of both the groups was 0.2-25.60 ng/ml. Though mean procalcitonin levels of patients of Group B (5.76±6.37 ng/ml) were found to be higher than that of Group A (4.81±6.60 ng/ml) yet this difference was not found to be significant statistically.
Duration of ICU stay was 4 to 27 days. Though mean ICU stay of patients of Group A (9.29±4.57 days) was higher than that of Group B this difference was not found to be significant statistically.
SOFA score of 56 patients of Group A and 55 patients of Group B could be assessed. Median SOFA score of patients of both the groups was 2.00, mean SOFA score of patients of Group A was 2.70±2.20 (range 0-9) while that of Group B was 2.53±1.63. On comparing SOFA score of patients of above two groups, difference was not found to be significant statistically.
CAM ICU score of 111 patients could be assessed. The majority of overall (68.5%) as well as Group A (76.8%) and Group B (60.0%) had negative CAM ICU scores. Though a higher proportion of Group B as compared to Group A had a positive CAM ICU score (40.0% vs. 23.2%), this difference was not found to be significant statistically.
There was no significant difference in the mortality of non-delirious patients.
Patients with delirium as compared to non-delirium had significantly higher values of APACHE-II (20.57±6.26 vs. 18.42±7.14) and significantly higher procalcitonin levels (5.84±6.25 vs. 3.42±6.57 ng/ml).
Table 4: Association of Delirium with Demographic Profile
Patients with delirium were found to be older as compared to non-delirium (41.57±9.99 vs. 35.87±11.81). This difference was found to be significant statistically. Proportion of females was higher among delirious as compared to non-delirious patients (54.3% vs. 47.4%), but this difference was not found to be significant statistically.
Delirium was less prevalent in Group A (16.6 percent) than Group B (31.4 percent), although the difference was not statistically significant. Melatonin administration did not significantly affect any of the other outcomes (p>0.05, all comparisons).
Discussion
Delirium is prevalent in all spheres of hospitalization, medical and surgical patients, more prominently in patients admitted to intensive care units. Owing to its multifactorial etiopathogenesis, multiple pharmacological and non-pharmacological methods have been described in various literatures for prevention and treatment of delirium.
Delirium is associated with various complications which may result in unfavorable outcomes. These complications may vary from minor complications like self-extubation, removal of catheters, weaning failure, increase length of ICU stay to increased mortality. Ely and coworkers(13) studied 275 mechanically ventilated medical ICU patients and determined that delirium was associated with a threefold increase in risk for 6-month mortality after adjusting for age, severity of illness, co-morbidities, coma, and exposure to psychoactive medications. The commonest factors significantly associated with delirium are dementia, increased age, co-morbidities, severity of illness, infection, decreased day to day activities, immobilisation, sensory disturbance, urinary catheterization, urea and electrolyte imbalance and malnutrition (14).
Frisk et al. (15) in 2004 conducted a study to assess the biochemical indicators of circadian rhythm of patients admitted in ICUs and found altered secretion patterns and reduction in the urinary metabolite of melatonin, 6-SMT (6-sulphatoxymelatonin). This indicated the possible disruption of this neurohormone in patients admitted in intensive care units. Andersen et al. (16) concluded that exogenous melatonin could be utilized to alleviate preoperative anxiety in surgical and critical care patients and more importantly, to decrease the emergence of delirium in the early postoperative period. In our study, 140 adult post-operative patients were studied to establish the preventive role of melatonin in delirium. Aghakouchakzadeh et al. (17) in 2017 conducted a comprehensive review to determine the effect of melatonin on delirium; they concluded that because exogenous melatonin can improve circadian rhythm and prevent delirium, melatonin supplementation could improve or manage delirium in the intensive care unit. Similarly, Yang et al. (18) in their review had found substantial preventative effects of melatonin on delirium .This investigation established a reason for the practice recommendations to recommend melatonergic medications for delirium prevention.
Out of 140 patients that we studied, 29 patients died during the trial, 35 were diagnosed with delirium and 76 had no delirium. Delirium was less prevalent in Group A (16.6 percent) than Group B (31.4 percent), although the difference was not statistically significant. This reduction is similar to the results found by Nishikimi et al. (19) in who found the melatonin agonist to be related to a trend toward shorter ICU stays, as well as significant reductions in the occurrence and duration of delirium in patients admitted to the ICU.
Sepsis and inflammation are important etiologies of delirium. Inflammatory biomarkers (procalcitonin and erythrocyte sedimentation rate) can be predictive of acute brain dysfunction and delirium. Hamza et al. (20) procalcitonin was significantly higher in their delirious group in univariant (0.9±0.6 vs. 0.4±0.4ng/mL, P<0.001) and multivariate analysis (OR= 35.59, CI (7.73- 163.76)). Similarly, McGrane S et al. (21) conducted a study in 87 non-intensive care unit (ICU) cohorts and found that higher levels of procalcitonin were associated with fewer delirium/coma-free days (odds ratio (OR), 0.5; 95% confidence interval (CI), 0.3 to 1.0; P = 0.04). Our study showed similar results with significantly higher procalcitonin levels in patients with delirium than those without delirium (5.84±6.25 vs. 3.42±6.57 ng/ml).
The Acute Physiology and Chronic Health Evaluation II score (APACHE II) provides a classification of severity of disease and is particularly used in the ICU to predict mortality. In our study, APACHE II scores were calculated for each patient at their admission in the ICU. The range of APACHE-II score of patients enrolled was 6 to 38. Patients of Group A and Group B had comparable APACHE-II Score (21.07±8.17 vs. 21.84±7.81). Patients with delirium as compared to non-delirium had higher values APACHE-II scores (20.57±6.26 vs. 18.42±7.14). This was similar to the findings of Hamza SA et. al.(17), who, in their observational study of 90 patients, found not only have higher APACHE scores but also that the APACHE-II scores had significantly high diagnostic performance in discrimination of delirium (AUC = 0.877, P= <0.001).
Another clinically important score is the Sequential Organ Failure Score (SOFA) score used to sequentially assess the severity of organ dysfunction in critically ill patient , is an objective score that calculates the number and the severity of organ dysfunction in six organ systems (respiratory, coagulation , liver, cardiovascular, renal, and neurologic). In a prospective cohort study on 400 consecutive patients admitted to the ICU Rahimi-Bashar et al. (22) found the SOFA scores were significantly higher in those with delirium (7.37 ± 1.17) than those without delirium (4.93 ± 1.70). Similarly in our study, SOFA score of patients with delirium (4.49±1.63) was found to be significantly higher than that of non-delirium (1.75±1.37). Hence the elevated SOFA and APACHEII scores in the delirium can assist in identifying at-risk patients for delirium and hence allow interventions to improve outcomes.
Aging is often associated with a disruption of the normal circadian cycle, which can also result in delirium. Thus, melatonin and its agonist may have a more significant influence on delirium in the elderly than in the young, Abbasi et al. (23) discovered that delirium is uncommon in a relatively young group. Thus, the relatively young age of our study sample and the enhancement of ICU care (such as decreased light, noise, and regular patient orientation) are the primary reasons for our study's low prevalence of delirium. Additionally, we found patients with delirium were older as compared to non-delirium (41.57±9.99 vs. 35.87±11.81).
As previously stated, the potential benefit of exogenous melatonin supplementation in reducing delirium incidence has been evaluated in non-ICU settings as well. While both the Sultan (24) and Jonghe (25) investigations examined whether melatonin may help postoperative patients avoid delirium, the de Jonghe study employed six times the amount of melatonin used in the Sultan study (3 mg versus 0.5 mg, respectively).
We suggest that individuals at risk of developing delirium, such as the elderly, should be investigated in future researches. Also, further studies are required comparing subgroups of medical, surgical, and trauma patients to determine which patients will benefit most from exogenous melatonin administration. Because plasma and urinary levels of melatonin are directly related to its concentration in the central nervous system, we also recommend monitoring melatonin levels in plasma or urine during the study and for follow-up to ascertain which subgroup of patients benefited most from exogenous melatonin supplementation to prevent delirium.
Conclusion
The study demonstrates there is decreased incidence of delirium in the patients who received exogenous melatonin, although this difference was statistically not significant (p=0.057). There was a statistically significant association of age with development of delirium (p=0.015). It has also been observed that the higher procalcitonin levels are associated with increased incidence of delirium (<0.001).
References
Cite as: Gupta K, Singh VK, Arshad Z, Singh GP. Effect Of Exogenous Melatonin on the Incidence of Delirium and Its Association with Severity of Illness in Postoperative Surgical ICU Patients. Southwest J Pulm Crit Care Sleep. 2022;25(2):7-14. doi: https://doi.org/10.13175/swjpcc030-22 PDF
Ali A. Mahdi MD, Charis Tjoeng DO, Vishal Patel MD, Serap Sobnosky MD
Dignity Health St Mary Medical Center
Department of Internal Medicine
Long Beach, California USA
Abstract
Methicillin-resistant Staphylococcus aureus (MRSA) bacteremia is a known cause of infective endocarditis. In this case report, we describe a patient with community-acquired MRSA bacteremia and subsequent mitral valve endocarditis. This patient was noted to be without commonly recognized risk factors for MRSA bacteremia, thus her likely source was skin colonization, with skin trauma facilitated by pediculosis infestation.
Case Presentation
An elderly woman was brought to the Emergency Department after being found down. A bystander called EMS after finding her lying on the ground next to a pool of emesis. Per EMS, the patient was found to have pinpoint pupils with Glasgow Coma Scale (GCS) 4-1-4, with only minimal improvement with a dose of naloxone. After admission she was noted to be afebrile, with a III/VI systolic murmur and an extensive infestation of lice in her hair. Urine toxicology screen was negative. CT radiography of her head was negative for acute intracranial pathology, with chronic ischemic changes. Blood cultures were drawn from two peripheral sites, but as the patient was afebrile without leukocytosis, she was not started on antibiotics. Her identity was later confirmed, and she was noted to be 72 years old with a history of homelessness. She had previously denied a history of IV drug abuse or previous surgeries, and was not noted to be hospitalized recently.
On the second day of hospitalization, her mentation improved, and she was described as coherent on exam. However, she became febrile to maximum temperature 38.5° C with a new leukocytosis to 14,500. Two of two blood cultures, drawn on admission, resulted in gram positive cocci with clusters, and she was started on empiric vancomycin therapy. The initial two blood cultures, as well as two repeat blood cultures later speciated to methicillin-resistant Staphylococcus aureus (MRSA). MRSA nares swab results were negative. However, as the patient was noted to have persistent pediculosis infestation, a possible source of MRSA bacteremia was skin colonization introduced to her bloodstream through excoriations. An infectious disease specialist was consulted, who recommended a transthoracic as well as a transesophageal echocardiogram.
Transthoracic echocardiography (TTE) revealed a moderate mobile vegetation on the posterior mitral valve leaflet (Figure 1A), as well as severe mitral regurgitation (Figure 1B).
Figure 1. Transthoracic echocardiography showing large vegetation on posterior leaflet of mitral valve (A) and severe mitral regurgitation resulting from large vegetation (B).
Left ventricular ejection fraction was reported to be 55-60%, with no other vegetations noted. On day five of hospitalization, the patient underwent transesophageal echocardiography (TEE), which revealed large vegetation on the posterior leaflet measuring 2.5 x 0.8 cm (Figure 3) causing severe mitral regurgitation (Figure 2).
Figure 2. Transesophageal echocardiography redemonstrating large vegetation on mitral valve (red arrow), measuring 2.5 x 0.8 cm.
A cardiothoracic surgery evaluation was obtained for mitral valve replacement, and she was deemed a surgical candidate.
In preparation for surgical intervention, cardiac catheterization was performed, which revealed no coronary artery disease. The patient’s pediculosis was noted to persist despite three topical treatments and two doses of oral ivermectin, and an additional dose of ivermectin was planned. Two repeat blood cultures resulted in no growth, and the patient was pending cardiothoracic surgery. However, on the day of surgery, the patient elected to leave against medical advice (AMA) despite extensive counseling. She had received 18 days total of IV vancomycin.
Discussion
MRSA continues to cause significant morbidity and mortality both in healthcare and community populations. S. aureus bacteremia can often cause complications, most concerning infective endocarditis, osteomyelitis, and sepsis. Incidence of community-acquired MRSA bacteremia, including healthcare-associated cases, has increased in recent years, surpassing rates of hospital-acquired infections globally (1-3). MRSA colonization increases the risk of MRSA infections and bacteremia; in a study of 29371 hospitalized patients, MRSA-colonized (per nasal swab) patients were 19.89 times more likely to develop bacteremia than non-colonized patients (4). Sites of S. aureus colonization include the nares, nasopharynx, skin, wound sites, and vascular catheters. Once colonized, traumatic injury or disruption can facilitate invasion of S. aureus into deeper structures of the skin, which can in turn lead to bacteremia.
There have been no documented cases of pediculosis as a contributor to MRSA bacteremia. However, lice have been identified as vectors for several pathogens, including Bartonella quintana, Rickettsia prowazekii, and Borrelia recurrentis (5). In particular, pediculosis has been shown to be associated with B. quintana seroconversion and bacteremia in a study of homeless individuals (6). B. quintana,is a gram negative bacteria transmitted by responsible for trench fever in World War I, during which it was transmitted by lice. More recently, it has been reported to cause bacillary angiomatosis, acute and chronic bacteremia, and endocarditis, with homeless persons and individuals with alcoholism at significant risk (7). Bartonella species including B. quintana have recently been described as emerging causes of culture-negative endocarditis (8). Notably, one case report documents a patient with a history of pediculosis, found to have culture-negative endocarditis. TEE revealed a 2.5 x 0.9 cm vegetation on the mitral valve and several small vegetations on the aortic valve. Serology was positive for both B. quintana and B. henselae, and rRNA sequencing confirmed B. quintana infection of both valves (9).
On TEE, our patient was shown to have a large vegetation on the mitral valve, measuring 2.5 x 0.8 cm in diameter. Given the high risk of embolization and severe mitral, valve replacement surgery was highly recommended. Per ID specialist, a six-week course of antibiotics was also recommended for complicated bacteremia. Unfortunately, the patient left against medical advice (AMA) before surgical intervention and before an appropriate duration of antibiotics.
The source of this patient’s bacteremia was initially unclear, as she did not have common risk factors for MRSA bacteremia. She denied IV drug use, was not recently admitted to a hospital or nursing facility, did not have any chronic conditions or prosthetic devices, and was found to have a negative MRSA nares swab. Thus, her source of infection was possibly skin colonization with MRSA, with introduction into her bloodstream facilitated by excoriations due to persistent pediculosis infestation. She was noted to have a significant amount of lice despite several topical and oral medications, and left AMA before completing a three-dose course of ivermectin.
Conclusion
In this case report, we describe a patient with community-acquired MRSA bacteremia and subsequent mitral valve endocarditis. In the absence of common risk factors, her likely source of infection was considered to be skin colonization, with skin barrier disruption from excoriations due to pediculosis.
References
Margaret Wat MD PhD, Jawad Bilal MD, Martin Chacon MD, Stephen Klotz MD, and Janet Campion MD
University of Arizona College of Medicine-Tucson
Tucson, AZ USA
History of Present Illness: A 29-year-old woman with past medical history of mixed connective tissue disease [lupus predominant], prior pulmonary embolism complained of a 2-week history of nonproductive cough. The cough began after her son was diagnosed with respiratory syncytial virus (RSV). Symptoms progressively worsened and now she is admitted from the emergency department (ED) with generalized weakness and progressive shortness of breath. Earlier in the day at an outside hospital, she tested positive for RSV, negative for COVID-19 and had normal O2 saturations and was discharged home. She has not received COVID-19 vaccine. Symptoms progressed, 911 called and in the ED, she was found to have temperature = 104°F, SpO2 = 64% on room air, and fasting blood sugar in the 40s. She was lethargic with visible respiratory distress and unable to answer questions.
Past Medical History:
Medications:
Social History and Family History
Physical Examination
Figure 1. Photographs of extremities taken during day 1 and 2 in the ICU.
With this patient's presentation, what is the most likely cause of the purpura? (Click on the correct answer to be directed to the second of six pages)