Hantavirus infection physical examination
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Basir Gill, M.B.B.S, M.D.[2] Furqan M M. M.B.B.S[3]
Overview
Physical examination findings in hantavirus infection vary depending on the clinical syndrome (hantavirus cardiopulmonary syndrome [HCPS] versus hemorrhagic fever with renal syndrome [HFRS]) and the phase of illness. During the prodromal phase, findings are nonspecific and include fever, tachycardia, and tachypnea. As the disease progresses, HCPS is characterized by signs of non-cardiogenic pulmonary edema and cardiogenic shock, whereas HFRS is characterized by flushing, petechiae, conjunctival injection, costovertebral angle tenderness, and signs of acute kidney injury.[1][2] Notably, the original description of HCPS in 17 patients from the 1993 Four Corners outbreak found that no patient had conjunctival hemorrhage, petechial rash, clinical signs of internal hemorrhage, or peripheral or periorbital edema — findings that are commonly seen in HFRS.[2]
Physical Examination
Appearance of the Patient
- Patients with hantavirus infection usually exhibit prostration and appear acutely ill.[3]
- The patient may be restless, fatigued, and irritable.
- In advanced cases, particularly during the cardiopulmonary phase of HCPS or the hypotensive phase of HFRS, the patient may be confused or comatose.[1]
Vital Signs
Vital sign abnormalities vary by syndrome and disease phase:
| Finding | HCPS | HFRS |
|---|---|---|
| Fever | Present in prodromal and cardiopulmonary phases | Present in 86% of patients; median onset day 1 of illness; median duration 4 days[4] |
| Tachycardia | Prominent during cardiopulmonary phase; 50% had heart rate ≥120 beats per minute at admission in the original HCPS series[2] | Relative bradycardia in 80% of PUUV patients; sinus bradycardia in 35% (median onset day 9.5)[4][5] |
| Tachypnea | 50% had respiratory rate ≥28 breaths per minute at admission[2] | Less prominent; may occur with pulmonary edema during oliguric phase |
| Hypotension | Hallmark of cardiopulmonary phase; present in all patients who died in the original HCPS series but in none of the survivors[2] | Occurs during the hypotensive phase due to vascular leakage[1] |
| Hypertension | Not typical | May develop during the oliguric phase (rebound hypertension)[1] |
Skin
HCPS
Skin findings are generally absent in HCPS caused by Sin Nombre virus (SNV). In the original 1993 series, no patient had petechial rash, conjunctival hemorrhage, or periorbital edema.[2]
- Patients infected with Andes virus (ANDV) may have petechiae on the axillae and extremities.[1]
- In severe HCPS with circulatory shock, mottling and slow capillary refill time are key bedside indicators of hypoperfusion that should prompt hemodynamic monitoring and inotropic drug titration.[1]
HFRS
- Erythematous flushing of the face, neck, and upper chest is an early and characteristic sign of HFRS (described as "three reds" in Chinese literature — red face, red neck, red chest).[3][7]
- Petechiae on skin and mucous membranes; more frequent in severe HFRS caused by Hantaan virus (HTNV) and Dobrava virus (DOBV); a third of PUUV patients have mild hemorrhages.[1]
- Ecchymoses may be present.[1]
- Periorbital edema may occur in HFRS.[2]
HEENT
Eyes
- Conjunctival injection: Common in both HCPS prodrome and HFRS febrile phase.[1]
- Conjunctival hemorrhage: Characteristic of HFRS; absent in HCPS.[2][1]
- Blurred vision and transient myopia: Found in up to 70% of patients infected with PUUV, caused by thickening of the lens. Myopia has a median onset on day 5 of illness and a median duration of 2 days.[4] In a detailed ophthalmological study, 87% had reduced visual acuity, 78% had myopic shift, 88% had decreased intraocular pressure, and 88% had thickening of the lens.[8] Patients infected with DOBV have a higher proportion of visual disturbances than those infected with PUUV.[1]
- Retro-ocular pain: Present during the HCPS prodrome.[1]
- Ocular findings combined with fever, headache, and thrombocytopenia may be pathognomonic for PUUV infection.[8]
Oropharynx
Cardiopulmonary
HCPS
Physical examination findings during the cardiopulmonary phase reflect non-cardiogenic pulmonary edema and myocardial depression:
- Bilateral crackles (rales) consistent with pulmonary edema; may initially be unilateral but rapidly becomes bilateral.[6]
- Signs of low cardiac output: weak pulses, cool extremities, mottling, prolonged capillary refill time.[1]
- Normal heart size on chest radiograph (indicating non-cardiogenic pulmonary edema).[6]
- The hemodynamic pattern of severe HCPS is distinct from both classic cardiogenic shock and septic shock: it is characterized by low cardiac index (range 1.6–3.0 L/min/m²), low stroke volume index (range 10.5–29 mL/m²), high systemic vascular resistance index (range 1,653–2,997 dyne·sec/cm⁵·m²), and low or normal pulmonary capillary wedge pressure.[1][9]
- Terminal events include sinus bradycardia, electromechanical dissociation, or ventricular tachycardia/fibrillation.[2]
- The legacy description of pericardial friction rub, S3 gallop, elevated jugular venous pressure, and lower limb edema as findings of "myopericarditis" in hantavirus infection is not well supported by the current literature. While myocardial depression and elevated NT-ProBNP concentrations are documented in PUUV-HFRS,[10] the predominant cardiac manifestation in HCPS is cardiogenic shock with low cardiac index rather than clinical pericarditis. ECG abnormalities in HFRS include T wave inversions (most common), ST segment changes, and relative bradycardia in 80% of PUUV patients.[5]
HFRS
- Two-thirds of PUUV-infected patients experience respiratory symptoms such as dry cough or dyspnea.[10]
- Pulmonary rales may be present during the oliguric phase if pulmonary edema develops.[1]
- More than half of patients with PUUV and DOBV have pathological pulmonary findings on chest x-ray with interstitial infiltrates and pleural effusions.[1]
- ECG abnormalities were detected in 18% of PUUV patients in a German study of 471 patients with nephropathia epidemica; in the Balkans, more than half of patients with PUUV and DOBV showed ECG abnormalities.[1][5]
Abdomen
- Abdominal pain can be intense and confused with acute abdomen in both HCPS and HFRS.[1][2]
- Costovertebral angle tenderness: Severe in HFRS, thought to be due to extensive extravasation of plasma into the retroperitoneal and peritoneal spaces; not typically seen in HCPS.[2]
- In HFRS, MRI of hospitalized PUUV patients has demonstrated fluid collections in virtually all patients — intraperitoneal, retroperitoneal, and pleural fluid.[1]
- Ascites was present in 40.9% of severe and 61.9% of critical pediatric HFRS cases caused by HTNV.[1][11]
- In the original HCPS series, CT scanning and ultrasound did not show abnormal fluid collection in the retroperitoneal space or elsewhere in patients with abdominal pain.[2]
Hemorrhagic Manifestations
Hemorrhagic findings are primarily a feature of HFRS and are generally absent in HCPS caused by SNV:[2][1]
| Finding | HFRS | HCPS |
|---|---|---|
| Petechiae (skin and mucosa) | Common; more frequent with HTNV and DOBV | Absent with SNV; may occur with ANDV (axillae, extremities) |
| Conjunctival hemorrhage | Common | Absent |
| Epistaxis | May occur | Absent |
| Gastrointestinal bleeding | May occur (hematemesis, melena) | Rare |
| Menorrhagia / metrorrhagia | May occur | Not reported |
| Ecchymoses | May occur | Absent |
| DIC / overt pulmonary hemorrhage | May occur in severe HFRS | Rare with SNV; may occur with ANDV |
| Periorbital edema | May occur | Absent |
Neurological Examination
- Headache (97%), blurred vision (40%), and vomiting (31%) are the most common neurological symptoms in PUUV-HFRS.[12]
- In a review of 811 PUUV-HFRS cases, 1% had severe neurological manifestations including meningism and cerebral hemorrhage (occurring during the first week) and epileptiform seizures and urinary bladder paralysis (developing during the second week).[12]
- Signs of CNS inflammation and PUUV-IgM in cerebrospinal fluid are common in acute nephropathia epidemica.[8][13]
- Altered mental status and confusion may occur in both HCPS (during shock) and HFRS (during the hypotensive or oliguric phase).[1]
Renal Examination
- HFRS: Oliguria or anuria occurs in 28% of patients (median onset day 6, median duration 2 days), followed by polyuria in 91% (median onset day 9, median duration 7 days).[4] Back and flank pain with costovertebral angle tenderness is characteristic.[2] Dialysis is required in approximately 15% of patients with DOBV, but in less than 5% of patients with PUUV.[1]
- HCPS: Renal involvement is typically minimal. None of the original 17 HCPS patients had the marked proteinuria followed by oliguria and renal insufficiency that is characteristic of severe HFRS, and serum creatinine did not rise above 2.5 mg/dL (220 μmol/L) in any patient.[2] However, mild creatinine elevation can occur, and both HCPS and HFRS can lead to renal failure.[1]
Distinguishing Physical Examination Features: HCPS vs. HFRS
The following table summarizes the key physical examination findings that help differentiate HCPS from HFRS:
| Physical Finding | HCPS | HFRS |
|---|---|---|
| Facial flushing | Absent[2] | Characteristic early sign ("three reds")[7] |
| Conjunctival injection | May be present in prodrome[1] | Common[1] |
| Conjunctival hemorrhage | Absent[2] | Common[1] |
| Periorbital edema | Absent[2] | May be present[2] |
| Transient myopia | Not typical | Up to 70% in PUUV[8] |
| Petechiae | Absent (SNV); may occur (ANDV)[1] | Common[1] |
| Costovertebral angle tenderness | Absent[2] | Severe (retroperitoneal plasma extravasation)[2] |
| Tachycardia | Prominent (≥120 bpm in 50%)[2] | Relative bradycardia in 80% (PUUV)[5] |
| Hypotension | Hallmark of cardiopulmonary phase[1] | Occurs during hypotensive phase[1] |
| Bilateral pulmonary crackles | Prominent (non-cardiogenic pulmonary edema)[6] | May occur during oliguric phase[1] |
| Oliguria / Anuria | Not typical | 28% of patients; median onset day 6[4] |
| Mottling / prolonged capillary refill | Key sign of circulatory shock[1] | Less prominent |
Pediatric Physical Examination
In a study of 206 pediatric patients with HFRS caused by HTNV, fever was present in 98.1%, stomachache in 63.1%, nausea/vomiting in 62.1%, headache in 45.1%, and backache in 66%. Bleeding symptoms (petechiae/ecchymosis, conjunctival hemorrhage, hematuria, pulmonary hemorrhage) were found in 47.1%. Hydropericardium was recorded in 9.1% of severe and 23.8% of critical cases. Hydrothorax was present in 31.8% of severe and 76.2% of critical cases. Ascites was present in 40.9% of severe and 61.9% of critical cases.[11]
Children with PUUV infection present more frequently with abdominal pain and vomiting, whereas adults present more frequently with arthralgia and visual disturbances.[14]
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 Vial PA, Ferrés M, Vial C, Valdivieso F, Mertz GJ, Godoy P (2023). "Hantavirus in humans: a review of clinical aspects and management". Lancet Infect Dis. 23 (9): e371–e382. doi:10.1016/S1473-3099(23)00128-7. PMID 37105214 Check
|pmid=value (help). - ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 Duchin JS, Koster FT, Peters CJ, Simpson GL, Tempest B, Zaki SR, Ksiazek TG, Rollin PE, Nichol S, Umland ET (1994). "Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease". N Engl J Med. 330 (14): 949–55. doi:10.1056/NEJM199404073301401. PMID 8189152.
- ↑ 3.0 3.1 Jiang H, Zheng X, Wang L, Du H, Wang P, Bai X (2017). "Hantavirus infection: a global zoonotic challenge". Virol Sin. 32 (1): 32–43. doi:10.1007/s12250-016-3899-x. PMID 28120221.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Pal E, Korva M, Resman Rus K, Fajs L, Strle F, Avšič-Županc T (2018). "Sequential assessment of clinical and laboratory parameters in patients with hemorrhagic fever with renal syndrome". PLoS One. 13 (5): e0197661. doi:10.1371/journal.pone.0197661. PMID 29791494.
- ↑ 5.0 5.1 5.2 5.3 Kitterer D, Greulich S, Grün S, Latus J, Henes J, Birkmeier S, Alscher MD, Braun N, Segerer S (2016). "Electrocardiographic abnormalities and relative bradycardia in patients with hantavirus-induced nephropathia epidemica". Eur J Intern Med. 33: 67–73. doi:10.1016/j.ejim.2016.06.001. PMID 27296590.
- ↑ 6.0 6.1 6.2 6.3 6.4 Llah ST, Mir S, Sharif S, Khan S, Mir MA (2018). "Hantavirus induced cardiopulmonary syndrome: a public health concern". J Med Virol. 90 (6): 1003–1009. doi:10.1002/jmv.25054. PMID 29322515.
- ↑ 7.0 7.1 7.2 Sargianou M, Watson DC, Chra P, Papa A, Starakis I, Gogos C, Panos G (2012). "Hantavirus infections for the clinician: from case presentation to diagnosis and treatment". Crit Rev Microbiol. 38 (4): 317–29. doi:10.3109/1040841X.2012.673553. PMID 22553984.
- ↑ 8.0 8.1 8.2 8.3 Vaheri A, Henttonen H, Voutilainen L, Mustonen J, Sironen T, Vapalahti O (2013). "Hantavirus infections in Europe and their impact on public health". Rev Med Virol. 23 (1): 35–49. doi:10.1002/rmv.1722. PMID 23027245.
- ↑ López R, Pérez-Araos R, Salazar Á, Ulloa-Morrison C, Pérez R, Llancaqueo M, Vial PA (2019). "Hemodynamic and pulmonary permeability characterization of hantavirus cardiopulmonary syndrome by transpulmonary thermodilution". Viruses. 11 (10): E900. doi:10.3390/v11100900. PMID 31569646.
- ↑ 10.0 10.1 Rasmuson J, Lindqvist P, Sörensen K, Hedström M, Blomberg A, Ahlm C (2013). "Cardiopulmonary involvement in Puumala hantavirus infection". BMC Infect Dis. 13: 501. doi:10.1186/1471-2334-13-501. PMID 24160911.
- ↑ 11.0 11.1 Li R, Sun J, Chen Y, Xiang Y, Gao Y, Yin Y, Jiang Y, Shen X (2023). "Clinical and laboratory features and factors predicting disease severity in pediatric patients with hemorrhagic fever with renal syndrome caused by Hantaan virus". J Med Virol. 95 (1): e28339. doi:10.1002/jmv.28339. PMID 36571133 Check
|pmid=value (help). - ↑ 12.0 12.1 Alexeyev OA, Morozov VG (1995). "Neurological manifestations of hemorrhagic fever with renal syndrome caused by Puumala virus: review of 811 cases". Clin Infect Dis. 20 (2): 255–8. doi:10.1093/clinids/20.2.255. PMID 7742425.
- ↑ Hautala N, Partanen T, Kubin AM, Kauma H, Hautala T (2021). "Central nervous system and ocular manifestations in Puumala hantavirus infection". Viruses. 13 (6): 1040. doi:10.3390/v13061040. PMID 34072819 Check
|pmid=value (help). - ↑ Echterdiek F, Kitterer D, Alscher MD, Segerer S, Braun N, Latus J (2019). "Clinical course of hantavirus-induced nephropathia epidemica in children compared to adults in Germany—analysis of 317 patients". Pediatr Nephrol. 34 (7): 1247–1252. doi:10.1007/s00467-019-04215-9. PMID 30874941.