Point-of-Care Ultrasound Techniques for the Small Animal Practitioner. Группа авторов
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Use of the AFAST AFS System in Nonhemorrhagic Effusions
Patients may become hypovolemic from nonhemorrhagic cavitary effusions and effusions within the retroperitoneal space. Analogous to the hypovolemic bleeding patient, nonhemorrhagic effusions are similarly categorized using the AFS system as “small‐volume effusion” (AFS 1 and 2 or with the modified AFS system <3) versus “large‐volume effusion” (AFS 3 and 4 or with the modified AFS system ≥3). The use of Global FAST helps detect effusions in these three major reservoir cavities and spaces that often are overlooked until effusions are advanced without ultrasound, radiography, and CT. The other two areas surveyed are the smaller reservoirs of the pericardial sac and lung (B‐lines). Smaller in that generally a patient cannot tolerate large volumes of pericardial effusion (heart fails) or many B‐lines representing alveolar‐interstitial edema (lungs fail). Global FAST should be routinely used in all volume‐depleted patients, as is advocated in human medicine (RUSH exam) (Perera et al. 2010), and discussed in more detail in Chapters 36 and 37.
Clinical Examples
An example of the manner in which AFAST with an AFS works in nontrauma monitoring is for the patient with pancreatitis that on day 1 has an AFS of 1 without any AFAST target organ abnormalities. The following day, the Global FAST approach is used, and the AFS has increased to 3. Moreover, Global FAST further evaluates for effusions using TFAST, volume status, and any lung complications using Vet BLUE, and no additional effusions other than the ascites are found. This is significant patient information because likely the disease process is worsening. The finding of an increase from AFS 1 to 3 dictates a more aggressively diagnostic and therapeutic pursuit. Without this approach as an extension of the physical exam, these changes are often missed until the complications advance even more and the patient becomes overtly clinical. In contrast, the following day the AFS has decreased to 0, likely reflecting a positive response to therapy, important information for the clinician as well as the client.
Additional practical Global FAST examples would include cases with right‐sided congestive heart (CHF) and making decisions on whether the patient requires therapeutic abdominocentesis as well as tracking ascites using the AFS for response to CHF therapy; and the use of the AFS postoperatively in vomiting septic abdomen cases to screen for abdominal‐related complications, including effusions and ileus or dehiscence, or thoracic‐related complications such as aspiration pneumonia or myocardial dysfunction, and so forth. The Global FAST approach screens these systems as part of its standardized protocol.
The use of AFAST and AFS in Dehydrated and Hypovolemic Patients
These subsets of veterinary patients often have no ultrasonographically visible free fluid until after they are resuscitated and rehydrated. In the dehydrated patient with a bowel perforation, the omentum is often adhered to the defect, with the resorption (recruitment) of any available free water from the abdominal cavity. Thus, the serious lesion (same for a “small‐volume bleed” from a mass) is not producing substantial free fluid until after rehydration and resuscitation. We use the mantra “Rehydrate, resuscitate, reevaluate with a minimum of at least one additional serial AFAST and AFS” within the next 2–4 hours. In humans with possible bowel injury, serial ultrasound examinations are recommended out to 12‐24 hours post‐admission (Mohammadi and Ghasemi‐Rad 2012) (Figure 7.9).
Pearl: Serial AFAST exams increase sensitivity in detecting peritonitis and “small‐volume bleed” suspects and should be performed four hours post admission, and again after resuscitation and rehydration. If the patient has not declared itself overtly surgical but remains a candidate, AFAST and AFS should be used serially for at least 12–24 hours and longer if patient status is questionable.
Use of AFAST for Canine Anaphylaxis
Gallbladder Wall Edema – Sonographic Striation
In 2009, the clinical utility of using point‐of‐care ultrasound for the rapid diagnosis of canine anaphylaxis (AX) was shown to be clinically helpful. Since the shock organ in dogs is the liver and gastrointestinal tract, hepatic venous congestion occurs rapidly (experimentally within minutes) due to massive histamine release within the portal circulation (Quantz et al. 2009; Caldwell et al. 2018; Hnatusko et al. 2019). As a result of massive histamine release, the intrahepatic venous sphincters tighten, thus causing the marked acute hepatic venous congestion along with degrees of gallbladder wall edema (intramural edema). The gallbladder change is generally easy to recognize during AFAST because the gallbladder is a fluid‐filled structure and the intramural edema appears as sonographic striation, alternating hyperechoic and anechoic layering, called the “halo effect” or “double rim effect” and more commonly the “gallbladder halo sign” (Quantz et al. 2009) (Figures 7.10 and 7.11). The sonographic striation is observed as an outer hyperechoic line (outer gallbladder wall) and inner hyperechoic line (inner gallbladder wall) with sonolucency (hypoechoic to anechoic) in between. In other words, a layering of white‐black‐white or white‐gray‐white (see Figures 7.10, 7.11, and 18.22).
The gallbladder wall edema is a more rapid (<2–4 minutes) sign of canine AX over traditional markers of liver enzyme elevation such as the alanine transaminase (ALT) level that may peak in as long as 2–4 hours (Quantz et al. 2009). It is important to note that there are additional causes of gallbladder wall edema (Table 7.5). In the acute setting, conditions that cause obstruction to venous and lymphatic return to the heart that also result in hepatic venous congestion are important rule‐outs and include pericardial effusion/cardiac tamponade and right‐sided congestive heart failure, such as dilated cardiomyopathy, pulmonary hypertension, and tricuspid valvular disease (Lisciandro 2014a,b, 2016a) (see Figure 18.22). In less acute conditions, primary gallbladder diseases (cholecystitis) and diseases that affect the gallbladder such as pancreatitis and cholangiohepatitis can also cause gallbladder wall edema. Other miscellaneous causes include severe hypoalbuminemia and third spacing (d'Anjou and Penninck 2015), immune‐mediated hemolytic anemia, post transfusion, and right‐sided volume overload from overresuscitation from fluid therapy (Nelson et al. 2010).
Rule‐outs are summarized in Table 7.5 with speculative pathogenesis and concurrent expected characterization of the caudal vena cava (see next section). The list is important to know to avoid “satisfaction of search error,” the failure to search for additional abnormalities, which is automatically avoided using the Global FAST approach. By failing to rule out these conditions, the patient may be incorrectly resuscitated to its detriment. For example, a canine AX case requires