Author: Dr. Charles Benson
59 year old male with history of OSA, HLD, DM, HTN, CAD, bradycardia s/p PPM, ESRD s/p pancreas/renal transplant transferred from OSH for acute severe abdominal pain with nausea/vomiting for day. He says the pain started 1 day ago and was located mostly in RLQ. He also endorses multiple episodes of NBNB emesis (10x) and inability to tolerate PO. He has never had pain like this before. It waxes and wanes and is worsened with movement and attempting to use the washroom. No dysuria or hematuria. Last BM 2 days ago was normal. No fevers, chills, chest pain, sob. Denies changes to urine output.
ESRD s/p renal and pancreas transplant (11/2020)
Bradycardia s/p PPM (1/2020)
Father: DM, HTN, “Heart disease”
Denies alcohol, tobacco, or recreational drug usage
Dust mite allergen
Armodafinil 250 mg
Atorvastatin 40 mg
Budesonide-formoterol 160-4.5 MCG/ACT inhaler
Bupropion 450 mg
Dulaglutide 1.5 mg/0.5 ML
Ergocalciferol 50,000 U
Famotidine 40 mg
Fluticasone 50 MCG/ACT
Furosemide 80 mg BID
Gabapentin 300 mg in AM and 600 mg PM
Lisinopril 10 mg
Mag-ox 800 mg TID
Metformin 500 BID
Montelukast 10 mg
Nifedipine 90 mg
Olopatadine HCL 0.7%
Sulfamethoxazole-trimethoprim 800-160 MG twice a week
Tacrolimus 9 mg BID
Constitutional: Positive for appetite change and diaphoresis. Negative for chills and fatigue.
Gastrointestinal: Positive for abdominal pain, nausea and vomiting. Negative for blood in stool, constipation and diarrhea.
Genitourinary: Negative for decreased urine volume, difficulty urinating, flank pain and frequency.
Musculoskeletal: Positive for back pain.
General: Acute distress d/t pain
HEENT: Atraumatic, normocephalic, trachea midline
Respiratory: Non-labored breathing, symmetrical chest extension
CV: Regular rate
Abdominal: +Distended, soft, significant and diffuse tenderness to palpation despite pain medications, no rebound tenderness or guarding
MSK: Spontaneous movements, ROM grossly intact
Extremities: 2+ pitting edema b/l, no cyanosis
Neuro: No focal neurological deficits
Skin: No rashes, skin warm and dry; ecchymosis on arms
Lactic acid WNL, CMV and BK virus pending, blood culture pending
Normal chest with no infiltrates or pulmonary edema
Few dilated loops of small bowel in the upper and mid abdomen. Correlate for partial obstruction or developing ileus.
US transplant kidney and pancreas with doppler
The transplant pancreas is identified in the right lower quadrant with fairly uniform isoechoic echotexture. No abnormal solid or cystic masses or lesions are seen. No extrahepatic pancreatic fluid collections are demonstrated.
Patent pancreas vasculature
The transplant kidney is well-identified in the right iliac fossa and is normal in size and echotecture. The transplant kidney measures 10.3 x 6.2 x 8.0 cm in its greatest dimensions. No abnormal solid or cystic masses, lesions or obstructive uropathy. No extra-renal fluid collections are seen. Arterial and venous flow are seen.
CT abdomen pelvis with contrast (1)
1. Appearance of edema in the colon extending from the region of the distal transverse colon to the distal descending colon almost up to the junction with the sigmoid. This was not present on the prior CT study performed at a different institution This could be due to can be seen with colitis which could be from infection, inflammation. Clinical correlation is however recommended to exclude other etiologies such as ischemia also in the appropriate clinical setting. The proximal visualized portions of the superior mesenteric artery, inferior mesenteric artery are grossly patent. Negative for acute diverticulitis.
2. Small volume intra-abdominal free fluid, increased from prior same day CT, possibly reactive.
CT Abdomen Pelvis without contrast (2)
1. No small or large bowel obstruction.
2. Right lower quadrant transplant kidney continues to enhance despite no IV contrast administration for this study. Most recent documented IV contrast administration November 28, 2022. Correlate for renal dysfunction.
3. Moderate volume complex free fluid throughout the abdomen, significantly increased from November 28, 2022. This could represent simple free fluid mixed with blood products/proteinaceous content of unknown etiology. If clinically necessary, consider fluid sampling for further evaluation.
Diagnosis: spontaneous intraperitoneal rupture of the urinary bladder
There are many causes of ascites, the most common in the US being cirrhosis with other common causes being malignancy-related and heart failure.
Signs and symptoms of ascites
Main complaint is generally abdominal distention which may be painless or associated with discomfort
Depending on cause can develop over the course of days to months
May also have weight gain, SOB, early satiety
Other signs and symptoms depend on underlying cause:
Hepatic - confusion, GI bleeding, stigmata of cirrhosis such as spider angioma, palmar erythema, jaundice, and abdominal wall collaterals
CHF - dyspnea, orthopnea,peripheral edema, JVD, pulmonary congestion or edema
Infection - fever, abdominal pain, AMS
Malignancy - weight loss, lymph nodes, night sweats
Chylous - steatorrhea, malnutrition, nausea, early satiety
Liver- abnormal liver enzymes, elevated INR, hypoalbuminemia, thrombocytopenia, anemia, or leukopenia
CHF - elevated BNP
SBP - leukocytosis, metabolic acidosis, and azotemia
Chylous - hypoalbuminemia, decreased gamma globulin levels, and lymphonia
All may have evidence of renal failure
No radiation risk or risk of contrast allergy or nephropathy
Should include dopplers to assess for portal vein dilation or reduction in blood flow
Can/should also include spleen
Easily evaluates for ascites and may provide further evidence of nodular liver or GI pathology
Serum-to-ascites albumin gradient
Cell count and differential
Total protein concentration
Culture and Gram stain
TB smear, culture, and adenosine deaminase activity
Cytology and CEA
Clear - uncomplicated ascites in the setting of cirrhosis is usually translucent yellow and may be completely clear if the bilirubin is normal and protein concentration is very low
Turbid or cloudy - 98% sensitive but 23% specific for detecting SBP
Opalescent - may point towards cirrhotic ascites with slightly elevated triglycerides
Milky - chylous ascites with a high triglyceride concentration that exceeds the serum concentration; is > 200 mg/dL and often greater than 1000 mg/d
Pink or bloody - usually with red cell concentration > 10,000 per mm3; most often due to traumatic tap but may be seen in cirrhosis, leakage of blood from previous tap, malignancy (HCC), or TB
Brown - deeply jaundiced patients with bilirubin concentration approximately 40% of the seum value; if greater than serum value then pt likely has ruptured gallbladder or perforated duodenal ulcer
Accurately identifies presence of portal hypertension and is more useful than the protein-based exudate/transudate concept
Gradient that is greater than or equal to 1.1 g/dL predicts portal HTN with 97% accuracy
Gradient < 1.1 indicates pt does not have portal HTN
Cell Count and Differential
Single most useful test to evaluate for infection
Consider abx treatment in any patient with a corrected neutrophil count >250 per mm3
Need to be corrected in pt’s with bloody samples - one WBC should be subtracted for every 750 RBC and one neutrophil for every 250 RBC
Total Protein Concentration
Can be classified as exudate if the TPC is >2.5 or 3 g/dL and transudate if below
Though less useful than SAAG still has value in differentiating causes of ascites
If corrected neutrophil count is > 250 cells/mm3 but meet two of the following criteria should warrant immediate evaluation to determine if bowel perforation into ascites has occurred
Total protein >1 g/dL
Glucose < 50 mg/dL
LDH greater than upper limit of normal for serum
May also help differentiate between cirrhosis and cardiac ascites
Cirrhosis - total protein < 2.5 g/dL
Cardiac - total protein > 2.5 g/dL
Back to our patient...
Labs with SAAG >1.1, protein <1, neutrophils < 250
So non-infected, portal HTN more likely liver in nature than cardiac given the transudative nature but LFTs wnl and no previous evidence of cirrhosis
Ventricular wall thickness is mild-moderately increased. Hyperdynamic left ventricular function. LV ejection fraction is visually estimated to be 65 to 70%.
Global RV systolic function is normal.
No significant valvular regurgitation.
PA systolic pressure not assessed due to an inadequate degree of tricuspid insufficiency.
IVC size is normal consistent with normal RA pressure
US of liver with doppler
No evidence for portal venous thrombosis as clinically questioned. Velocity within the portal venous system is sluggish.
Flow within the left hepatic artery is not seen possibly with limited technique secondary to body habitus and patient cooperation
Hepatomegaly with hepatic steatosis. No focal hepatic lesion
Moderate to large volume ascites.
IR transjugular liver biopsy
There is focal minimal liver related changes including mildly increased eosinophils, sinusoidal lymphocytosis and neutrophils.
The histopathological findings appear to be subclinical as these liver morphological changes are without accompanying significant abnormalities in liver enzymes.
Calculated sinusoidal pressure gradient of 2 mmHg (normal 1-5, with portal HTN being defined as greater than 5)
So what's the deal?
“Of the various compartments, the urine contains the greatest concentration of creatinine, estimated to be 100 times more concentrated than the serum. Thus, an ascites Cr:serum Cr ratio of over 1 is diagnostic of urinary ascites”
“Reabsorption of peritoneal Cr into the blood via diffusion, a phenomenon known as reverse peritoneal dialysis, increases sCr, resulting in pseudo-renal failure”
Does not improve with HD
Impression: a SUBTLE small strand of contrast appears extraluminal adjacent to the site of the ureterovesicular anastomosis, suspicious for urine leak. REcommend further evaluation with cystoscopy.
Urinary Bladder Rupture
Relatively rare condition but most commonly due to abdominal or pelvic trauma but may be spontaneous or iatrogenic in association with surgical or endoscopic procedures
Often blunt trauma in MVC
Extraperitoneal ruptures - pelvic fractures from compressive forces on pelvis causing rupture of the anterior and lateral bladder wall or from direct penetration of the bladdery by bony fracture fragments
Intraperitoneal ruptures - the full bladder is subjected to compressive forces in the lower abdomen
Nontraumatic Urinary Bladder Rupture
Iatrogenic - gynecological and colorectal surgery, urologic procedures, or foley catheter placement
Spontaneous - quite rare and associated with high mortality; associated with vaginal delivery, hemophilia, radiation, infection, and UTI
Has also been seen due to unnoticed overdistended bladder such as in an intoxicated individual
Occur in about 1.6% of pts with blunt abdominal trauma
Spontaneous or iatrogenic ruptures are usually intraperitoneal while traumatic tend to be extraperitoneal
Overall mortality has been as high as 10.8% in one database review
History and Physical
Most cases of bladder rupture have gross hematuria (77-100%)
Other symptoms include
Lower abdominal pain
Pelvic fracture should raise suspicion and fractures that involve the anterior arch or all four pubic rami significantly increase risk
Often associated with colon injuries
UA will show gross hematuria
Less than 1% will have UA containing less than 25 RBC
BUN and CR may be elevated due to peritoneal absorption of urine, especially if delayed presentation after the injury
Free fluid in the pelvis if intraperitoneal bladder rupture
Though may be difficult to determine blood vs urine in trauma
Pelvic trauma and blood at urethral meatus should raise concern for urethral injury
Do not place urinary catheter and obtain retrograde urethrogram
Stable patients with gross hematuria and pelvic fractures require retrograde cystogram
Should also be performed if symptoms suggest bladder rupture even without pelvic fracture
Fluoroscopy and CT cystography have similar sensitivity and specificity for bladder injury though CT is gold standard as it allows for assessment of other pelvic structures
Sensitivity 100% and specificity 99.6%
Unstable pts likely require surgical intervention, especially as most often in the setting of trauma
American urological association (AUA) guidelines recommend that intraperitoneal bladder ruptures be surgically repaired
Unrepaired may lead to peritonitis, sepsis, and renal failure
Uncomplicated extraperitoneal bladder injuries can be managed conservatively with catheter placement
Often left in place for 2-3 weeks