Intern Emerg Med DOI 10.1007/s11739-014-1094-3

CASE REPORT

An 85-year-old man with acute-onset of confusion and dyspnea after a fall: a diagnostic challenge Antonio Mirijello • Vincenzo Zaccone • Michele Impagnatiello • Anna Rita Larici Serena Stagliano` • Giovanni Addolorato • Raffaele Landolfi



Received: 22 April 2014 / Accepted: 4 June 2014 Ó SIMI 2014

Keywords Hip fracture  Acute corpulmonale  Dyspnea  Fat embolic syndrome

Differential diagnosis Dr Mirijello

Case presentation Dr Zaccone and Dr Impagnatiello An 85-year-old patient, previously in good general condition and with no relevant clinical history, presented to the emergency department (ED) because of rapidly worsening confusion and dyspnea that had suddenly manifested 1 h after a fall. The fall was reported by the patient as accidental, due to stumbling against a chair. The patient could remember the fall, and did not report any loss of consciousness. Patient’s relatives confirmed the dynamics of the fall. They decided to call for emergency help when acute dyspnea and confusion appeared. Upon arrival, the patient appeared dyspneic, dysarthric and severely confused, with right-side deviation of a buccal grimace. The right leg was shortened and externally rotated. Hypotension, tachycardia, tachypnea and peripheral oxygen desaturation were present (Table 1).

A. Mirijello  V. Zaccone  M. Impagnatiello  G. Addolorato (&)  R. Landolfi Department of Internal Medicine, Catholic University of Rome, Gemelli Hospital, Largo Gemelli 8, 00168 Rome, Italy e-mail: [email protected] A. R. Larici  S. Stagliano` Department of Radiological Sciences, Catholic University of Rome, Rome, Italy

This 85-year-old patient presented to the ED with cardiorespiratory and neurological symptoms that occurred acutely after a fall. An infectious disease seems to be unlikely due to the sudden onset of symptoms and the absence of chills, fever or organ-specific signs. Moreover, the absence of pre-existing symptoms and of any chronic diseases brings my attention toward the fall as the primum movens. A possible explanation of this symptomatology could be pulmonary embolism with consequent syncope and trauma. However, the patient did not have significant risk factors for, nor history of, thromboembolism. Moreover, in the chronological sequence, trauma was the first event; neurological and respiratory symptoms occurred after an hour. In addition, he and his relatives did not report any loss of consciousness. Indeed, shortening and external rotation of a leg after a fall are pathognomonic signs of hip fracture. Tachypnea and dyspnea could be the consequence of pain; however, in this case they would not be associated with oxygen desaturation. Hyperventilation could produce neurological symptoms (such as perioral paresthesia and Trousseau’s sign) due to respiratory alkalosis; however these signs should be peripheral. Hypotension and tachycardia could be the consequence of a post-traumatic hemorrhage. However, the acute appearance of dyspnea, tachycardia and hypotension could be also secondary to an acute pulmonary or circulatory problem. Diagnostic examinations are needed to performan appropriate differential diagnosis.

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Intern Emerg Med Table 1 Clinical data and instrumental examinations

Initial management and further investigations

Clinical examination Symptoms

Dr Zaccone and Dr Impagnatiello

Physical examination

Dyspnea, tachypnea, tachycardia Mental confusion Dysarthria Hearth: tachycardic, regular Lung: decreased breath sounds at bases CNS: deterioration of consciousness (GCS: 9/15, E3V2M4); right-side deviation of buccal rhyme Muscoskeletal system: right leg shortened and extra-rotated

Vital parameters Blood pressure Pulse rate Respiratory rate Peripheral oxygen saturation Laboratory tests pH pO2 pO2/FiO2 ratio pCO2 HCO3HB, at admission HB, lowest value PLT, at admission

100/60 mmHg 130 beats/min 36 breaths/min 90 % in 1.0 FiO2

Low High High Low

7.442 48.3 mmHg 97 25.3 mmHg 19.9 mEq/l 15.1 g/dl 9 g/dl 230.000/mm3

PLT, lowest value

100.000/mm3

n.v. 7.35–7.45 n.v. [ 65 mmHg n.v. [ 350 n.v. 38–42 mmHg n.v. 22–26 mEq/l n.v. 14–17 g/dl n.v. 14–17 g/dl n.v. 150–450.000/ mm3 n.v. 150–450.000/ mm3 n.v. \ 278 ng/ml n.v. \ 0.014 ng/ml n.v. \ 0.014 ng/ml

D-dimer [4,500 ng/ml T-troponin, at admission 0.084 ng/ml T-troponin, peak value 0.286 ng/ml (peak value) Instrumental examination Right femur X-ray Subcapital fracture of the right femur Electrocardiogram Sinus tachycardia with signs of acute corpulmonale (S1 Q3 T3) Brain CT scan Normal Chest X-ray Normal (at the admission) Diffuse interstitial involvement, bilateral basal opacities and bilateral pleural effusion (at the second day) Contrast-enhanced CT No arterial filling defects; a small scan of the lung consolidation of the posterior basal segment of the lower lobe and of the right medial basal segment with minimal bilateral pleural effusion Cardiac ultrasound Normal left ventricle; dilated and hypokinetic right ventricle with tricuspidal insufficiency and pulmonary hypertension (60 mmHg) CNS central nervous system, GCS Glasgow coma scale, PO2 partial pressure of oxygen, FiO2 fraction of inspired oxygen, PCO2 partial pressure of carbonic dioxide, HCO3 bicarbonate ions, CT computerized tomography

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In the ED, high flow oxygen (FiO2 100 %) was given to the patient. An electrocardiogram (ECG) showed signs of acute cor pulmonale [1] (Fig. 1). Blood gas analysis showed severe hypoxia and hypocapnia. D-dimer and HS-T-troponin were high (Table 1). Chest X-ray study and brain CT scan showed no significant abnormalities. A right femur X-ray study showed sub-capital hip fracture. A contrast-enhanced chest CT scan, performed to rule out pulmonary embolism, showed parenchymal consolidation and ground-glass opacities in the dependent areas of both lower lobes associated with minimal bilateral pleural effusion, along with an absence of arterial filling defects in the pulmonary arteries (Fig. 2a–d). Antibiotic treatment was started in the ED, and the patient was admitted to our Internal Medicine unit with a diagnosis of ‘‘hip fracture and pneumonia’’.

Final diagnosis and management Dr Zaccone and Dr Impagnatiello In our department, the patient showed a progressive worsening of respiratory and hemodynamic functions. These clinical features, together with the history of hip fracture and ECG signs of right ventricle overload, drew our attention to the hypothesis of a fat embolism syndrome (FES). Cardiac ultrasound showed a dilated and hypokinetic right ventricle, tricuspidal insufficiency, and pulmonary hypertension with a normal left ventricle. Repeated blood tests showed a further rise of troponin, a progressive decrease of platelets and anemia (Table 1). In the next 24 h, the respiratory distress worsened, and a chest X-ray study revealed bilateral alveolar opacities. These criteria led us to a diagnosis of FES [2] (Table 2). The patient was transferred to the ICU where non-invasive positive pressure ventilation and corticosteroids were started. The neurological status improved. On the fifth day after admission, the hip fracture was treated with an external fixation. Fortyeight hours after surgery, respiratory distress improved, with a progressive recovery. Troponin and platelet count returned to normal. The patient started pulmonary and motor rehabilitation, and was discharged in good general conditions. Discussion Dr Addolorato The present case represents a case of FES with hyperacute presentation after a traumatic fracture. Post-traumatic fat

Intern Emerg Med

Fig. 1 Twelve-leads ECG showing sinus rhythm, S1Q3T3, T inversion in V1–V5. Isolated ventricular extrasystole

embolism is a condition related to the entry of fat emboli into the circulation [3]. This leads to mechanical obstruction of arteries, and to vascular toxicity mediated by free fatty acids. Clinical manifestations, mainly related to cardio-respiratory, neurologic and cutaneous systems, are defined as the fat embolism syndrome. FES could have a highly variable clinical presentation, going from mild to fulminant forms [4]. Although FES is a frequent complication of trauma [5], generally it has a subclinical course, and it is probably underdiagnosed [6]. Dr Larici and Dr Stagliano` Radiographic abnormalities usually occur 24–48 h after trauma [7]. In most cases, fat embolism presents as microembolism [8] without any evidence of arterial filling defects at CT angiography. Common CT findings are focal or diffuse areas of consolidation and groundglass opacities that may be due to interstitial or alveolar haemorrhage, edema and chemical pneumonitis [9]. Small ill-defined centrilobular and subpleural nodules can be associated, presumably representing alveolar edema, microhemorrhage and inflammatory response secondary to ischemia [8]. Nevertheless, these features are nonspecific, and may resemble the acute respiratory distress syndrome following a variety of lung injuries [8] (pneumonia, pulmonary contusion, or cardiogenic pulmonary edema).

Dr Zaccone and Dr Impagnatiello In the emergency setting, FES diagnosis can be difficult to establish even when clinical signs are evident. Due to the lack of sufficiently sensitive and specific diagnostic tests, FES remains a diagnosis of exclusion to be performed on clinical-probabilistic terms [10] (Tables 2, 3, 4). Dr Mirijello The patient was admitted to our Department with a diagnosis of pneumonia. However, the acute respiratory failure after a hip trauma, as well as the absence of fever, in a previously healthy subject made this diagnosis unlikely. Moreover, ECG alterations [1] and neurological manifestations [11] were already present in the ED. At a critical review of the case, clinical features were found to fit with Schonfelds [2] criteria (Table 2). Also the clinical course, characterized by stabilization and marked improvement after surgery, was highly consistent with the diagnosis. Our patient did not show petechiae: however petechiae are present in only 50 % of cases [12]. Prof Landolfi The present case shows some interesting characteristics. First of all the hyperacute-onset of FES after a common type of hip fracture. Post-fracture FES generally occurs

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Intern Emerg Med

Fig. 2 Axial contrast-enhanced pulmonary CT images at mediastinal window setting at the level of the main pulmonary arteries (a), and the left (b) and right atrium (c) showing the absence of central and peripheral arterial filling defects and the enlargement of the right

atrium (c) (arrow). d Axial CT image at lung window setting showing ground-glass opacities in the left lower lobe, and areas of consolidation in the lateral and posterior basal segments of the right and left lower lobes. Bilateral mild pleural effusion is also evident

Table 2 Schonfeld’s criteria for the diagnosis of fat embolism syndrome: a cumulative score [5 is required for diagnosis

of elderly bone marrow tissue, together with some vascular frailty, have contributed to the entry of large amounts of fat material into the circulating system, this leading to early and severe clinical manifestations. These manifestations together with the ECG findings might have been interpreted as highly suggestive for pulmonary embolism, and led to heparin administration even before having CT scan confirmation of the clinical entity. However, the onset of symptoms, so soon after the traumatic event, made the hypothesis of post-traumatic thromboembolism unlikely, and drew our attention toward other possible mechanisms of acute cor pulmonare. The occurrence of FES after a single bone fracture is less frequent than after multiple bones fractures [16]. It is possible that FES may be underdiagnosed in the elderly population, due to multiple comorbidities, and the very likely high incidence of sudden death. It is conceivable that the substantially absence of previous chronic diseases and the good health condition contributed, in our case, to survival and a positive FES diagnosis.

Schonfeld’s criteria

Score

Petechiae

5

Chest X-ray changes (diffuse alveolar infiltrates)

4

Hypoxaemia (PaO2 \ 70 mmHg with an FiO2 100 %)

3

Fever ([38 °C) Tachycardia ([120 beats min-1)

1 1

Tachypnoea ([30 bpm)

1

The present case had a score of 9

12–24 h after traumatic event [3], while hyperacute/fulminant forms have been described in the setting of orthopedic surgery [13, 14] when the intramedullary bone rearrangement produces an acute increase of the intraosseous pressure, and trauma of the vascular structures determines an abrupt entry of fat material into the circulation [15]. It is conceivable that the higher adipose content

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Intern Emerg Med Table 3 Clinical manifestation of FES System

Pathophysiology

Symptoms

Cardiorespiratory

Fat embolization to the pulmonary arterial circulation: increase of dead space and FFA toxicity on lung parenchyma

Dyspnea

Fat embolization to the CNS: microvascular ischemia and hypoxemia due to acute respiratory failure

Mental confusion

Neurologic

Tachypnea Tachycardia

Fat embolization to subcutaneous vessels with extravasation of red blood cells

Other

FFA toxicity

Acute right heart failure Seizures Focal neurological signs (transient and completely reversible)

Petechiae (back, neck, axillary, conjunctives and oral mucosa): pathognomonic but incidence in only 50 % of cases Fever (up to 39.5 °C) Visual scotomata

FES fat embolic syndrome, FFA free fatty acids, CNS central nervous system

Table 4 Biochemical and instrumental diagnosis of FES Test

Result

Blood tests

Hypocalcaemia, hypoalbuminemia Increased D-dimer Anemia, thrombocytopenia Fat globules in urine Increase in circulating lipase and phospholipase A2

BAL

Fat containing scavenger macrophages

Chest X-ray

Normal, areas of hypodiafania, ground-glass areas, intraparenchymal hemorrhage, pleural effusion Thickening, nodules, areas of ground-glass attenuation, hemorrhage, pleural effusion

Chest CT scan

Conflict of interest

None.

Hypotension

Depression of consciousnesscoma Skin (50 % of cases)

Similarly to pulmonary embolism, FES could be defined as the ‘‘great simulator,’’ therefore it should be considered more frequently in the differential diagnosis of trauma patients, particularly in aged subjects.

Lung scintigraphy

Evaluation of the ventilation/perfusion ratio can show a pattern of subsegmental perfusion defect associated with a normal ventilatory pattern

Brain CT scan

Often normal

Brain MRI

Increase of the T2-signal that correlates with the development of neurological signs

References 1. Mirijello A, Pola R, Saviano L, Landolfi R. (2013) V1–V2–V3– V4 T wave inversion: left or right ventricle? BMJ Case Rep. doi:10.1136/bcr-2013-200331 2. Schonfeld SA, Ploysongsang Y, DiLisio R et al (1983) Fat embolism prophylaxis with corticosteroids. Ann Intern Med 99:438–443 3. Sevitt S (1977) The significant and pathology of fat embolism. Ann Clin Res 9:173–180 4. Van Besouw JP, Hinds CJ (1989) Fat embolism syndrome. Br J Hosp Med 42:304–311 5. Behn C, Ho¨pker WW, Pu¨schel K (1997) Fat embolism—a too infrequently determined pathoanatomic diagnosis. Versicherungsmedizin 49:89–93 6. Chan KM Tham KT, Chiu HS et al (1984) Post-traumatic fat embolism—its clinical and subclinical presentations. J Trauma 24(1):45–49 7. Han D, Lee KS, Franquet T et al (2003) Thrombotic and nonthrombotic pulmonary arterial embolism: spectrum of imaging findings. Radiographics 23(6):1521–1539 8. Bach AG, Restrepo CS, Abbas J et al (2013). Imaging of nonthrombotic pulmonary embolism: biological materials, nonbiological materials, and foreign bodies. Eur J Radiol 82(3):e120– e141 9. Nucifora G, Hysko F, Vit A et al (2007) Pulmonary fat embolism: common and unusual computed tomography findings. J Comput Assist Tomogr 31:806–807 10. Georgopoulos D, Bouros D (2003) Fat embolism syndrome: clinical examination is still the preferable diagnostic method. Chest 123(4):982–983 11. Jacobson DM, Terrence CF, Reinmuth OM (1986) The neurologic manifestations of fat embolism. Neurology 36:847–851 12. Tachakra SS (1976) Distribution of skin petechiae in fat embolism rash. Lancet 1:284–285 13. Pell AC, Hughes D, Keating J (1993) Brief report: fulminating fat embolism syndrome caused by paradoxical embolism through a patent foramen ovale. N Engl J Med 329:926–929 14. Glazer Onion DK (2001) Fat embolism syndrome in a surgical patient. J Am Board FamPract 14(4):310–313 15. Hoffmann S, Huemer G, Salzer M (1998) Pathophysiology and management of the fat embolism syndrome. Anesthesia 53(Suppl 2):1–80 16. Eriksson EA, Pellegrini DC, Vanderkolk WE et al (2011) Incidence of pulmonary fat embolism at autopsy: an undiagnosed epidemic. J Trauma 71(2):312–315

BAL bronchoalveolar lavage, CT computerized tomography, MRI magnetic resonance imaging

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An 85-year-old man with acute-onset of confusion and dyspnea after a fall: a diagnostic challenge.

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