Chronic Primary Splenic Torsion With

Peritoneal Adhesions in a Dog: Case

Report and Literature Review

Primary splenic torsion in dogs is uncommon and can occur in acute or chronic form. The
chronic form is difficult to diagnose because the clinical signs are vague and sometimes inter-
mittent. A dog with a history of diaphragmatic hernia repair two years previously presented with
chronic, vague clinical signs and an abdominal mass. The mass was revealed to be spleen on
ultrasonography. On exploratory laparotomy, the dog was found to have a splenic torsion of
approximately 180˚ with mature, fibrous adhesions retaining the spleen in a torsed position. A
splenectomy was performed, and the dog recovered uneventfully with complete resolution of
prior clinical signs. Prognosis for dogs with splenic torsion is good, although complications are
relatively common. J Am Anim Hosp Assoc 2000;36:390–4.

Niklos A. Weber, DVM Introduction

Splenic torsion is a relatively uncommon occurrence, and it is usually con-
sidered to be secondary to the gastric dilatation and volvulus (GDV) com-
C plex.1 Isolated primary splenic torsion (acute and chronic forms) occurs
rarely,2,3 and its etiology is poorly understood; but it is reported mostly in
large, deep-chested breeds, much like the GDV complex.4 Primary splenic
torsion is difficult to diagnose because of the nonspecific and sometimes
chronic or intermittent clinical signs and the relative rarity of the disorder.
Ultrasonography, especially color-flow Doppler, may be helpful in the diag-
nosis.5 Stabilization of the patient and splenectomy generally result in a
good prognosis, although complications such as cardiac arrhythmias, hem-
orrhage, coagulation disorders, and GDV are possible.

From the Bloomington Veterinary Hospital,
8830 Lyndale Avenue South,
Bloomington, Minnesota 55420.
Doctor Weber’s current address is
Skyway Pet Hospital, 7334 Skyway Avenue,
Paradise, California 95969.
Case Report
A six-year-old, spayed female golden retriever was presented with a prima-
ry complaint of mild depression and flinching when the left side of the head
was touched. The dog was mildly lethargic, her appetite was decreased, and
she usually kept her head tilted to the right but was not ataxic or circling. She
had undergone surgery two years previously for repair of a diaphragmatic
hernia that was not causing any clinical signs, but since the surgery she had
not seemed to the owners to be as active as before the surgery.
General physical examination revealed sensitivity when the left eye was
approached or the left side of the face was touched, severely erythematous
ear canals bilaterally, and a large, palpable mass in the cranial- to midab-
domen. The dog was mildly depressed and febrile (rectal temperature was
103.3˚ F). Ocular examination was normal bilaterally. The dog seemed to
hold her head tilted to the right, but no other neurological abnormalities were
noted. Complete otic examination was impossible because of the severe pain
and inflammation in the ear canals, and the owners were reluctant to have the
dog sedated. Abdominal radiographs revealed a large mass in the cranial- to
midabdomen. Complete blood count (CBC) revealed an inflammatory
leukogram with a left shift (white blood cells [WBC], 31.5 x103/µl; refer-
ence range, 6 to 16 x103/µl; neutrophils, 29.2 x103/µl; reference range, 3.2 to

390 JOURNAL of the American Animal Hospital Association

September/October 2000, Vol. 36
12 x103/µl; band cells, 5 x103/µl; reference range, 0 to 0.3
x103/µl) and mild anemia (hematocrit, 36.8%; reference
range, 38% to 55%). A serum biochemical profile showed
elevations in amylase (2,962 IU/L; reference range, 500 to
1,500 IU/L), lipase (1,032 IU/L; reference range, 0 to 1,000
IU/L), and nonfasting ammonia (140 µmol/L; reference
range, 0 to 98 µmol/L). A urinalysis was unremarkable. The
dog was placed on amoxicillina (15 mg/kg body weight, per
os [PO] tid), and ultrasonography was scheduled for the fol-
lowing day (day two). Chest radiographs prior to ultrasonog-
raphy were unremarkable, and the fasting serum ammonia
level was within the reference range.
Ultrasonography revealed a symmetrical, very large
spleen with a mixed echogenicity, a coarse liver of normal
size, and an area of hyperechoic tissue in the area of the pan-
creas, with a lobular area of hypoechogenic material within
it. This area was not aspirated, as the enlarged spleen sur-
rounded it and safe access to the area could not be ascer-
tained. Liver and spleen fine-needle aspirates were
performed and revealed splenic neutrophilic and histiocytic
inflammation and an unremarkable liver smear with copious
hemoglobin crystals. The owners were reluctant to have
exploratory laparotomy performed to evaluate the pancreas
and spleen, so enrofloxacinb (4 mg/kg body weight, PO bid
for 21 days) and metronidazolec (35 mg/kg body weight, PO
sid for 21 days) were added to the treatment regimen to treat
a possible pancreatic abscess or pancreatitis, as well as pos-
sible splenitis or localized peritonitis.
On day four, the dog presented for a recheck of the blood
work. The owners reported that the dog’s flinching was get-
ting worse and her appetite and activity levels were
unchanged. A CBC showed elevated leukocytes (26.7
x103/µl), neutrophils (22.4 x103/µl), and band cells (2.6
x103/µl). The hematocrit was decreased at 32%. Serum amy-
lase, lipase, and ammonia were within reference ranges, but
globulins were elevated (4.28 g/dl; reference range, 1.7 to
3.9 g/dl). Serum bile acids (pre- and two-hour postprandial)
were within reference ranges.
On day nine, the dog was flinching toward the left and
would not turn her head toward the left. She did, however,
have a better appetite and was more active. General physical
examination showed a slight head tilt toward the left but no
other neurological abnormalities. The abdominal mass
seemed a bit smaller at this time, and the dog’s temperature
was normal. The dog was anesthetized, skull radiographs and
a complete ear examination were performed, and cytopatho-
logical preparations of the otic discharge were made. The ears
had severe inflammation and mild hyperplasia in the horizon-
tal and vertical canals as well as bilateral ruptured tympanic
membranes. Discharge cytopathology showed many bacteria
(gram-negative rods) and a moderate number of yeast organ-
isms (Malassezia spp.). Skull radiographs showed bilateral
sclerosis and osteophytosis near the bullae. The ears were treat-
ed with miconazoled and dimethyl sulfoxide/fluocinolonee
plus enrofloxacinf bid and ear cleaning solutiong sid. The
Splenic Torsion in a Dog 391
dog was also started on oral prednisolone (0.66 mg/kg body
weight, PO bid for 5 days; then sid for 5 days; then every 48
hrs for 10 days) for otitis interna.
The dog presented for another recheck on day 16. She was
only rarely flinching at this time, and her appetite and activity
had increased. The size of the abdominal mass was
unchanged, and her temperature was normal. A CBC contin-
ued to show an inflammatory leukogram, with elevated leuko-
cytes (25 x103/µl), neutrophils (22.9 x103/µl), and band cells
(1.5 x103/µl). The hematocrit (41%) was within reference
range at this time. Exploratory laparotomy was again recom-
mended, and the owners elected to try conservative treatment
for another one to two weeks. On day 27, the ears were heal-
ing well, but the abdominal mass was unchanged.
Exploratory abdominal surgery and splenectomy were
performed 30 days after the original presentation. The
enlarged (15 by 15 by 10 cm) spleen was curled around (with
its hilus to the inside) and adhered to an 8-cm diameter mass
of omentum, and the head and tail of the spleen were adhered
to each other with an approximate 7-cm overlap. The side of
the spleen was also adhered to the duodenum for about 4 cm
of its length, fixing it in place. The degree of torsion in the
spleen was unclear, because the omentum covered the
splenic pedicle completely and the head and tail were
adhered together, but it appeared to be twisted approximate-
ly 180˚. Most of the adhesions present (including the duode-
nal adhesions) were mature, vascularized, fibrous tissues
containing vessels up to 1.0 mm in diameter, but some were
fibrinous, especially around the omentum. The spleen was
mottled dark red to black and was a lighter red on the surface
[Figure 1]. On cut section, the dark areas extended into the
parenchyma [Figure 2]. Also visible in Figure 2 is the area of
omentum within the spleen and the area where the head and
tail overlapped. The rest of the abdominal organs appeared
normal, including the pancreas and liver, and no evidence of
a cystic structure or pancreatitis was found.
Histopathology of the spleenh revealed extensive coagu-
lative necrosis with fibroplasia, neutrophilic inflammation,
and hemorrhage, consistent with splenic infarction. There
was no evidence of malignancy. The splenic capsule had
severe, diffuse fibrosis that extended into the surrounding
fat, and the entrapped omentum had regionally extensive
infarction with hemorrhage, fibrosis, and steatitis. The liver,
pancreas, and mesentery lymph node were normal on
histopathology.
The dog recovered well from surgery, and the otitis was
under control four weeks postoperatively. The owners
reported that she was more active four weeks postoperative-
ly than at any time since the surgery to repair the diaphrag-
matic hernia. The CBC was normal at that time as well. The
dog was continuing to hunt and do well two years after
surgery.
Discussion
Primary or isolated splenic torsion is an uncommon splenic
392 JOURNAL of the American Animal Hospital Association
Figure 1—Spleen from a golden retriever with chronic splenic
torsion and adhesions. Note the areas of light red congestion
(large arrow) and dark red to black ischemia (small arrow) in
the body of the spleen.
disease, seen in three of 87 (3.4%) cases of splenic diseases
requiring splenectomy in one study2 and seen in eight of
1,480 (0.5%) cases in another study.3 Most cases of splenic
torsion are secondary, usually to the GDV complex or neo-
plasia. Splenic torsion secondary to the GDV complex has
been reported to occur in 39 out of 193 (20%) dogs with
GDV in one study.1 Isolated primary splenic torsion general-
ly occurs in large- or giant-breed, deep-chested dogs, such as
Great Danes, German shepherd dogs, St. Bernards, collies,
and retrievers. Great Danes and German shepherd dogs have
been reported to be at significantly greater risk compared to
the general hospital population.5 There is no apparent age
predilection,6 but males have been reported to be affected
more than females.5,6
The etiology of primary splenic torsion is unknown. It has
been hypothesized that it occurs in conjunction with sponta-
neously resolving GDV or partial gastric torsion, which
leaves the spleen in a rotated position when the GDV
resolves.4 Another theory is that stretching of the suspensory
gastrosplenic, splenocolic, and phrenicosplenic ligaments
from GDV can cause a loosening of the splenic attachments
and may predispose the spleen to torsion.4 These two
hypotheses are supported by the reports of prior GDV
episodes in the histories of some dogs with isolated primary
splenic torsion.5 Other possible etiologies include simple
primary torsion of the spleen and torsion secondary to
splenic congestion after a GDV episode.4,5
Primary splenic torsion can present in acute and chronic
forms. Duration of clinical signs ranged from less than one
day (acute) to eight months, with a mean duration of about
6.5 days in one report.7 Median duration of signs has been
reported to be one day.5,6 The acute form is less common,
representing about 30% of all cases reported.4–6,8–10 Of the
remaining cases that presented with chronic signs, one-third
September/October 2000, Vol. 36
Figure 2—Cross-section of spleen from the same dog as in
Figure 1. Note the yellow omental tissue in the center of the
spleen, the area where the head and tail of the spleen are
adhered together (white arrowheads), and areas of
ischemia extending into the parenchyma (small, black
arrow).
of them presented in an acute episode requiring emergency
treatment.4–6,8–10
Acute splenic torsion usually causes severe, acute abdom-
inal pain and cardiovascular collapse in a matter of hours,
appearing clinically much like the GDV complex.
Discomfort and abdominal pain is frequently seen, as well as
retching, drooling, and weakness. If the dog is in a state of
collapse, signs of shock may be seen, such as tachycardia,
hypotension, and poor peripheral perfusion. An enlarged
spleen may be palpable, depending on the duration of the tor-
sion and the degree of pain and abdominal splinting that is
present. Blood work usually does not contribute to the diag-
nosis. Radiography usually shows a cranio- to midabdomi-
nal mass and sometimes localized or generalized peritoneal
effusion. Ultrasonography has been reported to show an
enlarged hypoechoic spleen with dilated splenic vessels and
splenic congestion,4 but the echogenicity and appearance of
the spleen can be variable, depending on the amount of
splenic blood flow remaining. Color-flow Doppler ultra-
sonography is more reliable, because it can show decreased
flow in the splenic veins and intravascular thrombi, even in
spleens with small blood vessels, subsequent to complete
vascular occlusion.5
The chronic form of primary splenic torsion usually pre-
sents with signs that are vague. The majority of dogs with
chronic splenic torsion present with depression, lethargy,
anorexia, and vomiting of several days’ duration. Anemia,
leukocytosis, hemoglobinemia, and elevated serum alkaline
phosphatase and alanine aminotransferase concentrations are
usually found after several days of chronic splenic torsion.
Elevated pancreatic enzymes are possible as well. Part of the
pancreatic blood supply comes from the splenic artery, so
September/October 2000, Vol. 36
pancreatic ischemia and pancreatitis can result from splenic
artery occlusion.11 Radiography and ultrasonography may
show an enlarged spleen, as with the acute presentation.
Recommended treatment for both forms of splenic tor-
sion is splenectomy after stabilization of the patient. The
splenic pedicle should not be untwisted in most cases, espe-
cially if the clinical signs are chronic, because this can cause
release of toxins (e.g., myocardial depressant factor or potas-
sium), microemboli, or bacteria into the bloodstream.
Splenic vessels should be ligated close to the spleen to avoid
occluding the pancreatic vascular supply. The spleen and any
other tissues appearing to be abnormal should be submitted
for histopathology to rule out the chance that the torsion was
secondary to neoplasia. Some cases of primary isolated
splenic torsion have been suspected to be secondary to spon-
taneously resolving GDV,7 and others have been reported to
occur after GDV surgery.5 Three cases were reported to have
developed GDV after splenectomy;5,8 therefore, gastropexy
concurrent with splenectomy is recommended. One dog did
well after the spleen was surgically repositioned,10 but repo-
sitioning generally is not recommended due to the high prob-
ability of toxemia and existing splenic thromboses.
Common complications associated with splenic torsion
include cardiovascular collapse (prior to surgery), ventricu-
lar arrhythmias (secondary to electrolyte imbalances,
microemboli, myocardial ischemia, or myocardial depres-
sant factors from splenic ischemia), and hemorrhage and
coagulation disorders (pre- and postoperatively). Other, less
commonly reported complications include disseminated
intravascular coagulation (DIC), thrombosis, or both; pan-
creatitis; GDV; and hemoglobinemia-associated nephrosis
(secondary to red blood cell destruction). Gastric dilatation
and volvulus after splenectomy has been reported more fre-
quently in the recent literature;4,5,8,11 it may be a more com-
mon complication to splenic torsion than previously
recognized. Gastric ischemia or necrosis is reported to be
possible, secondary to ligation of the splenic artery proximal
to the bifurcation of the left gastroepiploic artery,11 but no
cases have been reported in the veterinary literature. It is
believed that there may be enough collateral circulation to
that area of the stomach wall to prevent ischemia from occur-
ring.11,12
In cases of true primary splenic torsion, prognosis is
guarded to good. Acute splenic torsion cases have a more
guarded prognosis, because they potentially have more prob-
lems associated with shock and toxemia. The prognosis is
good for dogs with chronic torsion, as well as for those with
acute torsion that are treated appropriately, because early
treatment may lead to a better outcome.4 No clinical data has
been identified as positive or negative prognostic indica-
tors.5 In previously reported cases, 51 of 61 (83.6%) treated
dogs survived for at least one month postoperatively.4–6,8–10
Prior to 1990, a 74% (26/35)6,10 one-month survival rate was
reported, and after 1990 the rate increased to 96%
(27/28).4,5,8,9 This increase in treatment success has been
Splenic Torsion in a Dog 393
attributed to advances in pre- and postoperative monitoring,
greater understanding of emergency and critical care treat-
ment, increased use of ultrasound and color-flow Doppler
ultrasonography, and increased recognition of the disease.5
This case presented with chronic splenic torsion of
unknown duration. The spleen apparently had twisted and
then was retained in a twisted position by adhesion forma-
tion secondary to previous abdominal surgery, localized
peritoneal effusion, or both. The spleen may have had a pre-
disposition to torsion from breakdown of the splenic suspen-
sory ligaments due to the diaphragmatic hernia, the inciting
event that caused the hernia, the surgery to repair it, or a
combination of the above. It is possible that some of the
adhesions that held the spleen in torsion were secondary to
the diaphragmatic hernia. Prophylactic gastropexy was not
performed on this case, because the surgery was done before
the recommendations to perform prophylactic gastropexy
were published.8
Intra-abdominal adhesions form secondarily to all
abdominal surgical procedures, as well as many inflamma-
tory processes.13 Fibrinous adhesions are usually formed
soon after the inciting event and are removed by fibrinoly-
sis with plasmin in about one week.13 If the formation of
the adhesions is excessive (such as from severe serosal
trauma) or if the inciting cause remains for a long period of
time, the fibrinous adhesions are not removed rapidly
enough and they mature into fibrous adhesions in one to two
weeks.13 Even fibrous adhesions rarely cause problems,
unless they entrap bowel loops and cause obstructive bowel
disease.13 To the author’s knowledge, there have been no
other reported cases of adhesions of the spleen and sur-
rounding structures contributing to chronic splenic and
omental torsion.
Abdominal ultrasonography in this dog showed an
enlarged spleen, but it also showed a hyperechoic mass
between the spleen and stomach (in the area of the pancreas),
which had a fluid-filled structure within it. It is unlikely that
this area was a pancreatic abscess, because it was treated
conservatively, and pancreatic abscesses usually carry a poor
to grave prognosis even with surgery.14 It may have been an
area of compromised vasculature or necrosis in the spleen,
pancreas, or omentum, causing localized peritonitis or hem-
orrhage that subsequently resolved. Given the persistent
inflammatory leukograms, it is likely that the area was
inflammation, necrosis, or both, although the persistent otitis
could have caused the hematological abnormalities as well.
It is unknown whether any of the adhesions were caused
by the surgery two years previously, the localized peritoneal
effusion, or both. On exploratory laparotomy, there were
very mature adhesions between the spleen and duodenum
containing large (1.0-mm diameter) blood vessels within
them, and there were also areas of immature fibrinous adhe-
sions in the omentum. This may imply that the previous
surgery as well as the recent inflammation caused adhesions.
Because the spleen was fixed in place by the mature duode-
394 JOURNAL of the American Animal Hospital Association September/October 2000, Vol. 36

nal adhesions, it is possible that adhesions from the previous made from 87 canine splenic biopsies. J Sm Anim Pract 1995;
36:426–33.
surgery contributed to the chronicity of the splenic torsion. 4. Hurley RE, Stone MS. Isolated torsion of the splenic pedicle in a
Maturation to fibrous adhesions takes at least two weeks, but dog. J Am Anim Hosp Assoc 1994;30:2, 119–22.
no information is available about how long it takes large 5. Neath PJ, Brockman DJ, Saunders HM. Retrospective analysis of 19
blood vessels within peritoneal adhesions to form, so the cases of isolated torsion of the splenic pedicle in dogs. J Sm Anim
localized peritonitis may have contributed to the mature Pract 1997;38:9, 387–92.
6. Montgomery RD, Henderson RA, Horne RD, Bowers TS. Primary
adhesions as well. If the dog had suffered a partial splenic splenic torsion in dogs: literature review and report of five cases. Can
torsion for two years, it would explain the vague signs the Pract 1990;15:2, 17–21.
dog showed since the repair of the diaphragmatic hernia and 7. Brody RS. Spleen. In: Archibald J, ed. Canine surgery. 2nd ed. Santa
the resolution of those signs after splenectomy. Barbara, CA: Am Vet Pub, 1974:808–26.
8. Millis DL, Nemzek J, Riggs C, Walshaw R. Gastric dilatation-volvu-
lus after splenic torsion in two dogs. J Am Vet Med Assoc 1995;
a 207:3, 314–5.
Biomox; DelMarva Laboratories, Midlothian, VA
b 9. Goldsmid SE, Davis P, Pechman R. Successful derotation of a
Baytril; Bayer Corporation, Shawnee Mission, KS
c splenic torsion in a racing greyhound. J Sm Anim Pract 1994;
Metronidazole tablets, USP; Sidmak Laboratories, East Hanover, NJ
d 35:112–5.
Conofite; Pittman-Moore, Mundelein, IL
e 10. Stevenson S, Chew DJ, Koolba GJ. Torsion of the splenic pedicle in
Synotic; Fort Dodge Animal Health, Fort Dodge, IA
f the dog: a review. J Am Anim Hosp Assoc 1981;17:3, 239–44.
Baytril injectable; Bayer Corporation, Shawnee Mission, KS
g 11. Walshaw R. Hepato-biliary, pancreatic and splenic surgery. In:
Oticalm; DVM Pharmaceuticals, Miami, FL
h Lipowitz AJ, Caywood DD, Newton CD, Schwartz A, eds.
Histopathology read by Michael J. Tomlinson, DVM, Diplomate
Complications in small animal surgery: diagnosis, management, pre-
ACVP; Marshfield Laboratories, Marshfield, WI
vention. Philadelphia: Williams and Wilkins, 1996:435–43.
12. Hosgood G, et al. Splenectomy in the dog by ligation of the splenic
and short gastric arteries. Vet Surg 1989;18:2, 110–3.
References 13. Hardie EM. General abdominal surgery. In: Lipowitz AJ, Caywood
1. Brockman DJ, Washabau RJ, Drobatz KJ. Canine gastric DD, Newton CD, Schwartz A, eds. Complications in small animal
dilatation/volvulus syndrome in a veterinary critical care unit: 295 surgery: diagnosis, management, prevention. Philadelphia: Williams
cases (1986–1992). J Am Vet Med Assoc 1995;207:4, 460–4. and Wilkins, 1996:345–6.
2. Spangler WL, Culbertson MR. Prevalence, type and importance of 14. Harari J, Lincoln J. Surgery of the exocrine pancreas. In: Slatter D,
splenic diseases in dogs: 1480 cases (1985–1989). J Am Vet Med ed. Textbook of small animal surgery. 2nd ed. Philadelphia: WB
Assoc 1992;200:6, 829–34. Saunders, 1993:683–5.
3. Day MJ, Lucke VM, Pearson H. A review of pathological diagnoses