Lower Extremity Edema Ultrasound

Brief H&P:

$Ultrasound image of heart with depressed ejection fraction$

Depressed ejection fraction, image from The POCUS Atlas

An 44 year-old male with no reported medical history (though limited access to medical care) presents with lower extremity swelling. He states that the symptoms have been gradually worsening over the past 3 months. He notes occasional fatigue while at work but denies chest pain, shortness of breath, leg pain or changes in urination.

A point-of-care ultrasound is performed showing decreased left ventricular ejection fraction. The patient was admitted for further evaluation and management of new-onset congestive heart failure.

Algorithm for the Evaluation of Lower Extremity Edema with Ultrasound

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.

DVT
Cirrhosis
Soft Tissue

Nodular liver contour, ascites

Ascites

Cobblestoning

Longitudinal view of a ruptured Baker cyst

References

Trayes KP, Studdiford JS, Pickle S, Tully AS. Edema: diagnosis and management. Am Fam Physician. 2013;88(2):102-110.
Goyal A, Cusick AS, Bhutta BS. Peripheral Edema. [Updated 2022 Nov 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554452/
Smith, C. Clinical manifestations and evaluation of edema in adults. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed 2/11/2023.

This algorithm was developed by Dr. Huakang Huang. Huakang is an emergency medicine resident at UTHealth Houston.

Transfusion Reactions

Brief HPI:

A 28 year-old female with a history of systemic lupus erythematosus and end-stage renal disease without access to scheduled hemodialysis presents to the emergency department with 1 week of worsening dyspnea, fatigue and leg swelling. Her symptoms are reminiscent of prior episodes resolving with hemodialysis. On evaluation, vital signs are normal and laboratory tests demonstrate microcytic anemia (Hb 5.9g/dL) but no hyperkalemia. A plain chest radiograph is normal and the patient ambulates without hypoxia.

The patient was deemed to not meet any requirements for emergent hemodialysis. One unit of packed red blood cells was ordered for transfusion for symptomatic anemia. During transfusion, the patient developed worsening dyspnea and was found to be hypertensive and hypoxic. A chest radiograph was obtained and is shown below.

Pulmonary vascular congestion and bilateral pleural effusions.

The transfusion was discontinued, the patient was placed on non-invasive positive pressure ventilation, and emergent hemodialysis was initiated with subsequent resolution of presumed transfusion associated circulatory overload.

Algorithm for the Evaluation and Management of Transfusion Reactions

This algorithm was developed by Dr. Eric Madden, chief resident in emergency medicine at McGovern Med EM.

References

Carson JL, Triulzi DJ, Ness PM. Indications for and Adverse Effects of Red-Cell Transfusion. N Engl J Med. 2017;377(13):1261-1272. doi:10.1056/NEJMra1612789.
Delaney M, Wendel S, Bercovitz RS, et al. Transfusion reactions: prevention, diagnosis, and treatment. Lancet. 2016;388(10061):2825-2836. doi:10.1016/S0140-6736(15)01313-6.
Goel R, Tobian AAR, Shaz BH. Noninfectious transfusion-associated adverse events and their mitigation strategies. Blood. 2019;133(17):1831-1839. doi:10.1182/blood-2018-10-833988.
Osterman JL, Arora S. Blood product transfusions and reactions. Emerg Med Clin North Am. 2014;32(3):727-738. doi:10.1016/j.emc.2014.04.012.
Silvergleid AJ. Approach to the patient with a suspected acute transfusion reaction. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on September 01, 2019.)
Suddock JT, Crookston KP. Transfusion Reactions. January 2019.

Acute Kidney Injury

Hospital Course:

64 year-old female with a history of metastatic colonic adenocarcinoma was initially admitted for PO intolerance secondary to recurrent small bowel obstructions (associated with abdominal tumor burden). On hospital day six, the patient developed tachypnea, hypoxemia, hypotension and was intubated for respiratory distress. In the MICU, the patient was treated for acute hypoxic respiratory failure thought to be caused by aspiration (large volume bilious emesis prior to intubation despite NGT LCWS) vs. accumulating malignant pleural effusions vs. pulmonary embolism. Septic shock of a presumed pulmonary vs. intra-abdominal source was managed with vasopressors and broad-spectrum antimicrobials.

On hospital day fourteen, an elevation in the serum creatinine was noted. Known nephrotoxic agents include iodinated contrast on hospital day five, and vancomycin. The patient’s vasopressor requirement had decreased to norepinephrine 6mcg/kg/min (previously requiring four vasopressors). Over the next six days, the serum creatinine continued to trend upwards associated with a decrease in urine output (0.3-0.5mL/kg/hour). Intravenous crystalloid and colloid administered liberally based on central venous pressure and ultrasound of the inferior vena cava did not impact urine output.

Laboratory Studies

Hospital day	19	18	17	16	15	14	3
Creatinine	1.72	1.59	1.46	1.32	1.24	1.09	0.75
Vancomycin	23.5	28.5	36.3	45.5	47.7		22.1

Urine electrolytes:

Una: 10
Ucr: 180
Uk: 13
Ucl: 22
Uur: 265
FeNa: <1%

UA: 3+LE, 1+ blood, 36WBC, 14RBC, 3+ bacteria, amorphous crystals

Imaging:

CT Abdomen/Pelvis with IV contrast

Within the retroperitoneum, the left kidney is small and atrophic and demonstrates limited peripheral enhancement. The left renal artery is also poorly visualized.
Severely dilated loops of small bowel, including a segment within the left lower quadrant that may represent a closed loop obstruction.
There is a large (16.4 cm in largest diameter) subphrenic fluid collection in the left upper quadrant. A second large (14.2 cm in largest diameter) intraabdominal fluid collection lies inferior and anteriorly.

Assessment:

Oliguric acute renal failure in the setting of convincingly pre-renal urine studies which was not responsive to adequate crystalloid and colloid volume resuscitation. The patient had a normal ejection fraction on a recent echocardiogram, and while the patient was hypoalbuminemic (presumably from poor nutritional status and PO intolerance), urine output was not even transiently responsive to colloid administration. While the patient had recent administration of intravenous contrast, the elevation in serum creatinine occurred more than one week later. Further, the elevated vancomycin trough was likely a consequence rather than the etiology of worsening renal failure. AKI was likely secondary to renal artery compression from mass effect associated with abdominal metastases. There was evidence of a similar process affecting the left kidney, which was severely atrophic. The patient declined further evaluation, which would have included a renal ultrasound.

Definition of Acute Kidney Injury: ¹

Elevation of serum creatinine > 0.3mg/dL in 48h
Elevation of serum creatinine > 1.5x baseline in 7d
Oliguria (UOP < 0.5mL/kg/hr) > 6h

Staging of Acute Kidney Injury: ¹

Stage	Creatinine	UOP
1	1.5-1.9x	<0.5mL/kg/hr for 6-12h
2	2.0-2.9x	<0.5mL/kg/hr for >12h
3	3.0x or RRT	<0.3mL/kg/hr for > 24h

Management of Contrast-induced AKI: ²

Administer lowest dose
Use iso-osmolar, or low-osmolar contrast
Volume expansion (NaCl, NaHCO3)
PO NAC questionable benefit but likely harmless

Differential Diagnosis of Acute Kidney Injury: ³

NOTE: Algorithm revised in November, 2017. The prior version is no longer supported but remains available here.

Evaluation of AKI: ⁴

Condition	Urinalysis	Casts	FeNa (%)
Pre-renal	Normal	Hyaline	<1
Intra-renal
ATN	Mild proteinuria	Pigmented granular	>1
AIN	Mild proteinuria, Hb, WBC	WBC casts, eosinophils	>1
GN	Moderate/severe proteinuria, Hb	RBC casts	<1
Post-renal	Normal	Crystals	>1

References:

Kellum, J. A., Lameire, N., KDIGO AKI Guideline Work Group. (2013). Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical care (London, England), 17(1), 204. doi:10.1186/cc11454
Lameire, N., Kellum, J. A., KDIGO AKI Guideline Work Group. (2013). Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (Part 2). Critical care (London, England), 17(1), 205. doi:10.1186/cc11455
Lameire, N., Van Biesen, W., & Vanholder, R. (2005). Acute renal failure. Lancet, 365(9457), 417–430. doi:10.1016/S0140-6736(05)17831-3
Thadhani, R., Pascual, M., & Bonventre, J. V. (1996). Acute renal failure. New England Journal of Medicine, 334(22), 1448–1460. doi:10.1056/NEJM199605303342207
WikEM: Acute kidney injury

Lower Extremity Edema

HPI:

51 year-old male with a history of HTN, DM and chronic alcohol abuse presenting with lower extremity swelling. He notes one month of progressive, bilateral lower extremity swelling, in the past two weeks associated with increasing pain and redness and is now no longer able to ambulate due to pain. He denies fevers/chills, chest pain or shortness of breath. He also denies orthopnea and paroxysmal nocturnal dyspnea. He states that he has not had these symptoms prior to one month ago. On review of systems he denies nausea/vomiting, abdominal pain, and changes in bowel or urinary habits. He has a history of GI bleeding (unknown treatment) but denies hematemesis, hematochezia or melena. He has previously experienced alcohol withdrawal, which manifested as tremors, but no hallucinations or seizures.

PMH:

HTN
DM
Chronic EtOH abuse

PSH:

None

FH:

Unknown

SHx:

Drinks 1-2 pints of alcohol daily, last drink this morning.
Denies current tobacco or drug abuse, no prior IVDA.

Meds:

None

Allergies:

NKDA

Physical Exam:

VS:	T	37.6	HR	86	RR	16	BP	128/84	O2	99% RA
Gen:	Adult, non-obese male, lying in bed. Tremors noted in upper extremities.
HEENT:	PERRL, EOMI, no scleral icterus. Mucous membranes moist.
CV:	RRR, normal S1/S2, no additional heart sounds, JVP 3cm above sternal angle at 30°.
Lungs:	CTAB, no crackles.
Abd:	Soft, non-distended, with normoactive bowel sounds. Liver edge palpated 1cm below costal margin at mid-clavicular line, non-tender. No rebound/guarding.
Ext:	Warm, well-perfused with 2+ distal pulses (PT, DP). 3+ pitting edema symmetric in bilateral lower extremities to knee. Erythema and warmth bilaterally extending from ankles to mid-shin. Mild tenderness to palpation. No pain with passive dorsiflexion. 3x3cm shallow ulceration below medial malleolus on right lower extremity without underlying fluctuance or expression of purulent material. No venous varicosities noted. Decreased sensation to light touch below knee bilaterally.
Rectal:	Normal rectal tone, brown stool, guaiac negative.
Neuro:	Alert and oriented, CN II-XII intact, gait intact, normal FTN/RAM.

Labs/Studies:

CBC: 7.4/13.1/39/180
Creatinine: 0.84
Albumin: 4.3
BNP: 28

Imaging:

Venous Lower Extremity Ultrasound

No DVT.
Pulsatile flow in bilateral EIV (external iliac veins) suggestive of elevated right heart pressure.

Assessment/Plan:

51M with HTN, DM, EtOH abuse presenting with lower extremity edema. Chronic bilateral lower extremity edema likely secondary to chronic venous insufficiency perhaps related to OSA given ultrasound findings of pulsatile flow in EIV’s. Doubt systemic cause: no evidence of heart failure on exam and normal BNP, no stigmata of cirrhosis and normal albumin, normal creatinine. Also, no evidence of DVT on ultrasound though bilateral DVT unlikely. Bilateral cellulitis also unlikely as the patient is afebrile without leukocytosis, however the patient was started on antibiotics including ceftriaxone and TMP/SMX given erythema, warmth and tenderness to palpation. The patient received benzodiazepines which eased withdrawal symptoms and he was admitted for continued treatment.

Mechanisms of Lower Extremity Edema: ¹

Differential Diagnosis of Lower Extremity Edema: ^1,2

Evaluation:

History ^1,2

Duration: acute (<72h) vs. chronic
Pain: DVT, CRPS, less severe in venous insufficiency
Systemic Disease
- Cardiac: orthopnea, PND
- Renal: proteinuria
- Hepatic: jaundice, ascites
Malignancy: lymphedema
Improvement with elevation/recumbency: venous insufficiency
OSA: snoring, daytime somnolence
Medications: B-blocker, CCB, hormones, NSAID’s

Physical Exam ^1,2

Distribution: unilateral, bilateral, generalized
Quality: pitting, non-pitting
TTP: DVT, cellulitis
Varicose veins: venous insufficiency
Kaposi-Stemmer: inability to pinch dorsum of foot at base of 2nd toe (lymphedema)
Systemic Disease
- Cardiac: JVD, crackles
- Hepatic: ascites, scleral icterus, spider angiomas
Brawny, medial maleolar involvement: venous insufficiency

Key Features Distinguishing Cellulitis: ³

Typically unilateral and acute
Often with systemic symptoms (fever, leukocytosis)
Risk Factors: immunosuppression, previous episodes, DM, PVD

References:

Trayes, K. P., Studdiford, J. S., Pickle, S., & Tully, A. S. (2013). Edema: diagnosis and management. American family physician, 88(2), 102–110.
Ely, J. W., Osheroff, J. A., Chambliss, M. L., & Ebell, M. H. (2006). Approach to leg edema of unclear etiology. Journal of the American Board of Family Medicine : JABFM, 19(2), 148–160.
Keller, E. C., Tomecki, K. J., & Alraies, M. C. (2012). Distinguishing cellulitis from its mimics. Cleveland Clinic journal of medicine, 79(8), 547–552. doi:10.3949/ccjm.79a.11121
WikEM: Pedal edema

Renal Failure in Cirrhosis

CC:

Consult for acute kidney injury

HPI:

63M with a history of liver cirrhosis of cryptogenic etiology, portal vein thrombosis, and esophageal varices s/p banding (2011) who was admitted to an OSH for altered mental status and hypotension requiring dopamine and was transferred to this facility for a higher level of care.

The nephrology service was consulted for elevated serum creatinine concerning for AKI. The patient has a baseline creatinine of 1.1 (3/2013), 1.9 on transfer and continued worsening to peak of 2.6 today.

PMH:

Asthma
COPD
Cirrhosis (PVT, encephalopathy)
Inguinal hernia (recurrent)

PSH:

Appendectomy
Bilateral inguinal hernia repair

FH:

Non-contributory

SHx:

Married
Denies t/e/d use

Meds:

albumin 25g i.v. q.6.h.
erythromycin 1,000mg p.o. q.1.h.
fluticasone-salmeterol 1 puff b.i.d.
lactulose 45g p.o. q.6.h.
neomycin 1,000mg p.o. q.1.h.
pantoprazole 40mg i.v. daily
rifaximin 550mg p.o. b.i.d.
sodium benzoate 5g p.o. b.i.d.

Allergies:

Sulfa

Physical Exam:

VS:	T	37.4	HR	90	RR	15	BP	86/48	O2	97% RA
Gen:	Chronically ill-appearing.
HEENT:	PERRL, scleral icterus, MMM
CV:	RRR
Lungs:	CTAB
Abd:	+BS, soft, non-tender, non-distended
GU:	Large ascites filled scrotum, testicles/inguinal canal not easily palpated
Ext:	Warm, well-perfused
Skin:	No palmar erythema, no vascular spiders
Neuro:	AAOx4, CN II-XII grossly intact

Labs:

BMP: 134/4.5/103/20/41/3.0/106 (Ca 9.3, Mg 3.7, PO4 2.4)
LFT: AST 89, ALT 33, TB 26.6, CB 16.1, Alb 2.7
NH4 167

Imaging:

Pleural Effusion

Large right pleural effusion with underlying compressive atelectasis.

Cirrhosis and Portal Hypertension

Shrunken/nodular liver with sequelae of portal hypertension including perisplenic collaterals, and splenomegaly.

SMV Thrombosis

Near-total thrombosis of the portal vein extending down to superior mesenteric vein.

B/L Inguinal Hernias

Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

Large Right Inguinal Hernia

Large volume abdominal ascites with a large amount of fluid extending into the bilateral inguinal canals.

CT Abdomen/Pelvis (PVT)

Assessment/Plan:

63M with a history of liver cirrhosis of cryptogenic etiology, recently with hypotension prior to transfer to this facility and increase in creatinine from 1.9-3.0 on current admission (from baseline 1.1).

These findings indicate acute kidney injury, likely hepatorenal syndrome vs. acute tubular necrosis 2/2 prolonged hypotension. Plan to discontinue diuretics and start albumin challenge (1g/kg/day divided q6h x2d). Will also check UA, urine Na/cr/urea/eos, renal US (evaluate obstruction, kidney size). Start midodrine/octreotide for underlying HRS.

Neuro: Intermittent confusion. Lactulose, rifaximin, benzoate.
Resp: 2L NC. ABG 7.36/51/87/27.7/+2. CXR: Large R effusion.
CV: Levo 0.075. Midodrine 15 TID. MAPs 60, HR 80s.
GI: NPO/NGT. TPN.
Renal: See above.
Heme: Coagulopathy, keep INR <2.5
ID: Afebrile. No abx.
Endo: Euglycemic

Renal Failure in Cirrhosis:

Renal failure in cirrhosis is associated with higher mortality both before and after transplant. The main causes of renal failure in cirrhosis are detailed below, with particular attention to an entity unique to cirrhosis: the hepatorenal syndrome.¹

Disorder	Pathogenesis	Diagnosis	Management
HRS	Dilation of splanchnic arteries initially compensated by increased CO eventually decompensates with activation of mechanisms to preserve ECBV (RAAS, SNS, ADH) leading to fluid retention (ascites, edema) and renal failure due to intrarenal vasoconstriction.Bacterial translocation and the resulting inflammatory response may contribute to splanchnic vasodilation (through production of vasoactive factors like NO).	Serum creatinine > 1.5mg/dl- Not reduced with 1g/kg albumin No confounding factors (2d off diuretics, no nephrotoxic agents, no shock, no e/o intrinsic renal disease) Type 1: doubling creatinine > 2.5mg/dL in <2wk Type 2: stable, slower progression	Vasoconstrictor therapy- Albumin Portasystemic shunting Renal replacement therapy Prevention Norfloxacin Albumin
Intrinsic renal	Some causes of liver disease are also associated with intrinsic renal pathology (ex. GN associated with HBV, HCV).	Proteinuria, hematuria Renal bx Active urinary sediment	Antiviral therapy if appropriate
Pre-renal AKI	Hemorrhage (GIB), fluid losses (excess diuresis, diarrhea from lactulose).	Suspected from patient history Low FENa, bland urine sediment	Hemorrhage: replace volume with fluids, blood products. Control bleeding. Discontinue diuretics, administer fluids if tolerated
ATN	Severe ischemic or toxic (NSAID’s, nephrotoxic medications)	Renal tubular epithelial cells favor ATN (granular casts common in ATN, HRS)	Withdraw therapy Avoid nephrotoxic agents

Pathophysiology of Hepatorenal Syndrome:

Evaluation:

The evaluation of suspected renal failure in patients with cirrhosis involves assessment of renal function for evidence of acute impairment, as well as analaysis of urine for protein or active sediment to suggest intrinsic renal disease (possibly warranting renal ultrasonography or biopsy). Additionally, patients should be evaluated for evidence of bacterial infection including assessment of ascites if present as SBP produces a more severe form of the inflammatory vasodilation mechanism suspected to play a role in HRS.

Treatment:

For renal failure not caused by the hepatorenal syndrome, identification and management of the underlying cause is critical (intrinsic renal disease, hypovolemia/hemorrhage, nephrotoxicity, infection). For suspected HRS, management is dependent on the acuity and setting. In the intensive care unit, vasoconstrictor therapy (norepinephrine, vasopressin) in association with albumin is effective in the treatment of HRS.^2,3 In less acute settings, a combination of midodrine, octreotide and albumin improves renal function and is associated with lower short-term mortality.⁴ Alternatives for patients who do not respond to medical therapy include TIPS, dialysis and transplant.

Summary:

Renal failure in ESLD is due to the causes, complications or management of cirrhosis and has important implications, with HRS in particular offering the worst prognosis.⁵ Early recognition and management is critical to improving outcomes.

References:

Ginès, P., & Schrier, R. W. (2009). Renal failure in cirrhosis. The New England journal of medicine, 361(13), 1279–1290. doi:10.1056/NEJMra0809139
Singh, V., Ghosh, S., Singh, B., Kumar, P., Sharma, N., Bhalla, A., Sharma, A. K., et al. (2012). Noradrenaline vs. terlipressin in the treatment of hepatorenal syndrome: a randomized study. Journal of hepatology, 56(6), 1293–1298. doi:10.1016/j.jhep.2012.01.012
Kiser, T. H., Fish, D. N., Obritsch, M. D., Jung, R., MacLaren, R., & Parikh, C. R. (2005). Vasopressin, not octreotide, may be beneficial in the treatment of hepatorenal syndrome: a retrospective study. Nephrology, dialysis, transplantation, 20(9), 1813–1820. doi:10.1093/ndt/gfh930
Esrailian, E., Pantangco, E. R., Kyulo, N. L., Hu, K.-Q., & Runyon, B. A. (2007). Octreotide/Midodrine therapy significantly improves renal function and 30-day survival in patients with type 1 hepatorenal syndrome. Digestive diseases and sciences, 52(3), 742–748. doi:10.1007/s10620-006-9312-0
Alessandria, C., Ozdogan, O., Guevara, M., Restuccia, T., Jiménez, W., Arroyo, V., Rodés, J., et al. (2005). MELD score and clinical type predict prognosis in hepatorenal syndrome: relevance to liver transplantation. Hepatology (Baltimore, Md.), 41(6), 1282–1289. doi:10.1002/hep.20687

Brief H&P:

Algorithm for the Evaluation of Lower Extremity Edema with Ultrasound

Gallery

References

Brief HPI:

Algorithm for the Evaluation and Management of Transfusion Reactions

References

Hospital Course:

Laboratory Studies

Imaging:

CT Abdomen/Pelvis with IV contrast

Assessment:

Definition of Acute Kidney Injury: 1

Staging of Acute Kidney Injury: 1

Management of Contrast-induced AKI: 2

Differential Diagnosis of Acute Kidney Injury: 3

Evaluation of AKI: 4

References:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs/Studies:

Imaging:

Assessment/Plan:

Mechanisms of Lower Extremity Edema: 1

Differential Diagnosis of Lower Extremity Edema: 1,2

Evaluation:

History 1,2

Physical Exam 1,2

Key Features Distinguishing Cellulitis: 3

References:

CC:

HPI:

PMH:

PSH:

FH:

SHx:

Meds:

Allergies:

Physical Exam:

Labs:

Imaging:

Pleural Effusion

Cirrhosis and Portal Hypertension

SMV Thrombosis

B/L Inguinal Hernias

Large Right Inguinal Hernia

CT Abdomen/Pelvis (PVT)

Assessment/Plan:

Renal Failure in Cirrhosis:

Pathophysiology of Hepatorenal Syndrome:

Evaluation:

Treatment:

Summary:

References:

Definition of Acute Kidney Injury: ¹

Staging of Acute Kidney Injury: ¹

Management of Contrast-induced AKI: ²

Differential Diagnosis of Acute Kidney Injury: ³

Evaluation of AKI: ⁴

Mechanisms of Lower Extremity Edema: ¹

Differential Diagnosis of Lower Extremity Edema: ^1,2

History ^1,2

Physical Exam ^1,2

Key Features Distinguishing Cellulitis: ³