Elderly Heart Failure - Essay Sample

Introduction

The prevalence and incidence of heart failure (HF) continue to increase especially in older people, constituting a critical geriatric problem. In the elderly patient, the etiopathogenic, epidemiological and even clinical characteristics of HF differ significantly from those present in the youngest patient, but the treatment that is applied derives from the results of clinical trials with little participation of elderly patients. Beyond cardiopathy, it is essential to evaluate the patient as a whole, taking into account the interrelation between HF and the different geriatric syndromes characteristic of the elderly patient. This case presents a case analysis of a 30-year-old woman admitted to the Emergency Department due to fever and urinary discomfort after being discharged due to eutocic delivery. The participant must arrive at the diagnosis and answer the various questions with the information of the case and complementary tests.

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Background, Current Disease, and Physical Exploration

Personal History

• Allergic to penicillin.
• No known hypertension or diabetes mellitus
• Dyslipidemia in dietary treatment.
• Denies toxic habits.
• Primary autoimmune hypothyroidism in substitution treatment since 2011.
• Eutocic delivery of a single gestation 40 + 1 weeks on 06/15/2014 without immediate complications. Hyperemesis gravidarum.
• Baseline situation: active and independent. Suitable for the patient's age.
• Surgical interventions: removal of the cutaneous nevus on four occasions, one being dysplastic.
• Chronic treatment: levothyroxine 150 mcg (75 mcg after delivery): 1 first/day 40 mg iron proteinsuccinylate: 1 vial per day.

Current Illness

A 30-year-old woman who came to the Emergency Room due to poor general condition with a thermomelated fever of 38.5 C that was accompanied by dysfunctional urinary incontinence, frequency, and pain in the right lumbar region of 24 hours of evolution. The patient has presented nausea but without vomiting. No cough or expectoration or other accompanying symptoms. The patient was discharged on the second day after eutocic delivery without immediate complications.

Physical Exploration

• Blood pressure: 110/90 mmHg.
• Heart Rate: 90 beats/minute.
• Temperature: 38.8 C.
• 100% oxygen saturation.
• Weight 63.5 kg, size 1.72m. BMI: 21.46 Kg/m2.
• Cardiac auscultation: rhythmic noises at 90 bpm and without murmurs.
• Pulmonary auscultation: conserved vesicular murmur.
• Abdomen: soft and depressible, painful hypogastric palpation and fist positive right renal percussion.
• Lower extremities: edema with fovea up to the knee without signs of thrombosis. Gynecological examination: engorged breasts without signs of infection. Wide and elastic vagina. Flow is not smelly.

Supplementary Tests

Analytical Admission: glucose 81, creatinine 0.99, sodium (Na +) 139, potassium (K +) 4.2, PCR 11.39, hemoglobin 10.6, hematocrit 32.4%, leukocytes 13380 (neutrophils 77%), platelets 275,000. INR 0.93. Abnormal and sediment: pH 7, hemoglobin 593 erythrocytes/field. Leukocytes 1912 leukocytes/field. Bacteria 2019/uL. Pyuria.

Other analytical findings on admission: Baseline ACTH 1180, basal cortisol 3.3. TSH 8.08, T4 1.16, T3 1.8. Na + plasma 124, Na + urine 15, chlorine plasma 89, chlorine urine 10, urine osmolality 294, blood osmolality 288. Anti-striated muscle/myocardial antibodies: negative. Anti-adrenal antibodies: high positive.

Chest x-ray: congestive hills. Increase of the Broncho-vascular plot.

Bilateral costophrenic sinus impingement with a volume decrease in the right hemithorax.

ECG: sinus tachycardia at 100 bpm. PR 0.12sec. Narrow QRS with indeterminate axis and morphology of BIRTH. T negative waves in II, III and aVF. Deep T waves in precordial leads.

Transvaginal ultrasound: involuted uterus with a collapsed cavity. No impression of remains. Abdominal ultrasound: a moderate amount of intraperitoneal free fluid predominantly in the flanks and right iliac fossa, and in lesser amount in the lower pelvis. Kidneys of normal size and structure, without dilatation of the excretory system. Severe right pleural effusion with practically total pulmonary atelectasis and moderate left pleural effusion.

Transthoracic echocardiography (Cardiology): biventricular dysfunction without dilatation of cavities (LVEF 35%). Mild mitral insufficiency. Signs of low cardiac output. Absence of indirect symptoms of severe pulmonary hypertension.

Coronary angiography: coronary arteries without significant lesions.

Ventriculography: dilated left ventricle with irregular contour on the inferior side (small aneurysms). FEVI 25%. Moderate MI TDVI 24 mmHg. Severe ventricular dysfunction.

Endomyocardial biopsy: fragment of the myocardium with slight hypertrophic features without the presence of inflammation or granulomas. Interstitial fibrosis is not seen. No deposit of iron or glycogen. No inflammation that suggests myocarditis is identified.

Cardiac MRI: cavities dilation is not observed. Normal myocardial thickness. Severe left ventricular dysfunction (LVEF 35%). No intra-myocardial edema is observed. Delayed negative enhancement, which makes the diagnosis of myocarditis and ischemic heart disease very unlikely.

Microbiology: blood culture: negative at six days of incubation. Urine culture: Escherichia Coli> 100,000 CFU/mL sensitive to gentamicin, fosfomycin, cotrimoxazole, and amoxicillin-clavulanic acid. Serology parvovirus B19: Ac IgG and Ac IgM parvovirus B19 negative.

Evolution

The patient enters Gynecology with the diagnosis of acute pyelonephritis in puerpera. Urine cultures and blood cultures are requested, and intravenous treatment is started with gentamicin 80 mg every 8 hours, clindamycin 900 mg every 8 hours, fluid therapy (1500 cc daily) and analgesia. On day 23/06 the patient presented nausea, vomiting with dizziness and hypotension (TA 97/73 mmHg) and 500 ccs of extra serum therapy and metoclopramide were administered. The next morning the patient persists with an affectation of her general state with a dyspnea sensation despite presenting 100% saturation and is attributed to anxiety crisis. But in the following hours, the patient presents poor general condition with mucocutaneous pallor, sweating, and peripheral coldness as well as tachycardia and tachypnea. The examination highlights: FC 120 bpm, FR 40 rpm, BP 80 / 30mmg, Sat O2 88% pulmonary auscultation: bibasal hypoventilation marked on the right lung base. Chest radiography is performed urgent, where bilateral pleural effusion is seen; abdominal ultrasound urgent-te, where free intra-abdominal fluid and bilateral pleural effusion can be seen. Analytically it highlights Na + 128, K + 6.3, NT-proBNP 9162, Hb 9.2, Dimer D 8421, PCR 37.42, procalcitonin 4.50, GOT 1190, GPT 377, TSH 7.690, T4 0.96, pH 7.20, pCO2 19, HCO3 12, lactate 4 and glucose 40. Given the hemodynamic deterioration of the patient with respiratory claudication, she was admitted to the ICU with the diagnosis of metabolic acidosis secondary to sepsis of urinary origin due to E. coli.

The patient was admitted to the ICU on the afternoon of 24/06 with unstable hypotension and signs of tissue hypoperfusion requiring initial respiratory support with non-invasive mechanical ventilation and administration of 3 doses of hydrocortisone due to the acute pulmonary edema. ECG is performed where negative T waves are seen in the inferior and precordial side, as well as elevation of markers of cardiac damage with a peak of CKMB 21.6 and troponin T 279 and NT-proBNP 12626. Urgent cardio is performed where dysfunction is seen severe systolic with global hypokinesia, dilatation of cavities with LVEF 10% and cardiac output of 2 liters/minute. Given that the patient is in cardiogenic shock, treatment with vasoactive dobutamine and norepinephrine is instituted to maintain systolic tensions of 80 mmHg and improvement in cardiac output at 5 l / minute and LVEF 35%. With the suspicion of myocarditis / ischemic heart disease, cardiac catheterization with ventriculography and endomyocardial biopsy, cardiac MRI, serology of parvovirus B19 and cardiac immunology that are all negative are performed, which is why the picture is attributed to possible peripartum cardiomyopathy complicated with sepsis of urine origin (Westhoff-Bleck et al., 2018). Treatment is started with bromocriptine, treatment with gentamicin is maintained, and trimethoprim-sulfamethoxazole is associated. The patient improves clinically, with a resolution of the bilateral pleural effusion, improvement of the infectious analytical parameters and cardiac output, allowing the progressive withdrawal of the vasoactive drugs and on 01/07 she moves to the Cardiology plant.

Initially, in the Cardiology plant, the evolution is favorable, allowing to initiate betabloqueantes and IECAs to low doses. In the control echocardium, improvement of systolic dysfunction with LVEF 35% was observed. But on the night of 03/07, the patient presented nausea and dizziness with hypotension of 70 / 40mmHg. Analytical is performed with these alterations: creatinine 1.65, urea 58, Na + 117, K + 6.4, which are confirmed. Bromocriptine and trimethoprim-sulfamethoxazole were discontinued (completed antibiotic cycle) in case the alterations were secondary to drugs, and corrective measures of hyperkalemia and serum therapy are administered.

Given that the patient at 24-48 hours persists with the symptoms of dizziness, nausea, and hypotension and with peak analytical alterations on 06/07 with creatinine 1.99, urea 90, Na + 115, K + 7.4, ACTH and basal cortisol are requested and IV hydrocortisone is administered when acute adrenal insufficiency is suspected (Bancos, Hahner, Tomlinson & Arlt, 2015). The patient improves progressively with the treatment. Endocrinology is consulted, which classifies acute adrenal insufficiency in patients with stress due to urinary sepsis and cardiogenic shock due to peripartum cardiomyopathy. The patient received steroid treatment in the ICU, so the box had remained masked. Given the hemodynamic stability of the patient and the resolution of the ionic alterations, it is discharged on 08/07/2014.

Treatment at discharge: omeprazole 20 mg 1c/24h, ramipril 2.5 mg 1c/24h, bisoprolol 2.5 mg 1c /24h, furosemide 40 mg 1/2 c/24h, levothyroxine 75 mcg 1c/24h, hydrocortisone 20 mg 1c/ 8h.

Evolution at discharge: after four months, control echocardiography was performed, where improvement was seen with LVEF 52%. At the endocrinological level, the analytical results confirmed the condition as acute adrenal insufficiency of autoimmune origin. At nine months, the patient is asymptomatic and with active and independent life.

Diagnosis

• Urinary sepsis due to Escherichia Coli
• Cardiogenic shock due to peripartum cardiomyopathy with severe systolic dysfunction
• Acute adrenal insufficiency-Addisonian crisis

Discussion

Peripartum cardiomyopathy is defined as idiopathic cardiomyopathy that presents as heart failure secondary to systolic dysfunction of the left ventricle that occurs towards the end of pregnancy or in the months after childbirth. It is a diagnosis of exclusion, which requires ruling out other causes of heart failure or preexisting cardiomyopathy aggravated by pregnancy. The specific physiopathological mechanisms are not yet entirely known. Hilfiker-Kleiner et al. postulate that prolactin may play an essential role since at the cardiac level there are enzymes such as cathepsin D that generates free radicals by cleaving prolactin in a 16 KDal fragment. This fragment causes apoptosis, vasoconstriction, dysfunction, and dilation of cavities.

Another mechanism would be the immune system, identifying the peripartum cardiomyopathy as a graft-versus-host disease where the heart is the immunological target due to the mother's reaction to the antigens of the greater...