Acute Pancreatitis in Dogs

Key Facts

- Acute pancreatitis occurs when pancreatic proteases are prematurely activated

and subsequently released into the abodominal cavity and systemic circulation

- The condition should be suspected in any middle-age or old dog that has

a sudden onset of vomiting, anorexia, and depression.

- The history, physical findings, radiographic findings, and laboratory test

results are used together to make the clinical diagnosis.

- Treatment commenly requres complete cessation of oral intake of food in add

in addition to administration of intravenous fluids and antibiotics.

- Surgery is indicated for pancreatic phlegmon, psedocyst, and abscess.

Physiology

- »ç¶÷ÀÇ °æ¿ì pancreas´Â B.WÀÇ 1% ¹Ì¸¸.

´Ü¹éÁú »ý»ê ´Æ·ÂÀº LIver ¿Í RESÀÇ 13 ¹è.

Exocrine, Endocrine ±â´ÉÀÌ ÀÖ´Ù.

Exocrine pancreatic protease - trypsin, chymotrypsin, elastase,

carboxypeptidase A & B, phospholipase A

- õýíô ¿ÜºÐºñ¼±À¸·Î ºÎÅÍ ÝÂÝôµÇ´Â proteaseÀÇ AutodigestionÀ» ¸·´Â ¹æ¹ý

衁. Inactive precursors³ª proenzyme ÇüÅ·ΠºÐºñ, transport, synthesis ÇÑ´Ù.

遁. Duodenum¿¡¼­ enterokinase-mediated enzymeÀÌ °ü°­ Ȱ¼ºÀ» °ÅħÀ¸·Î

trypsinogenÀÌ trypsinÀ¸·Î Àüȯ µÈ´Ù.

鑁. ¸·°áÇÕ ¼Ò±â°üÀÌ ¼±¹æ¼¼Æ÷ ¼¼Æ÷Áú·Î ºÎÅÍ proezymeÀ» ºÐ¸® ½ÃÅ´.

鱁. Trypsin inhibitor°¡ ¼¼Æ÷ ¼Ò±â°üÒ® Á¸Àç (¹Ì·®ÀÇ È°¼º trypsinÀ» inactivate)

ꁁ. Blood plasma°¡ alpha-antitrypsin, alpha-macroglobulin,

antichymotrypsin °°Àº antiprotease¸¦ ÇÔÀ¯

- Á¤»óÀûÀ¸·Î Ç÷·ù³» proenzyme ÇüÅ·Πprotease°¡ ÝÂÝôµÇ°í trypsin°ú chymotrypsin

³óµµ°¡ »ó½Â ÇÑ´Ù.

Pathology

衁. ºÎÁ¾¼º ÃéÀå¿°Àº mildest form

; °£Áú¼º ºÎÁ¾°ú neutrophil°ú lymphocyte·Î µÈ ¿°Áõ»ê¹°ÀÌ ÀÖ´Ù.

¼±¹æÁ¶Á÷°ú Duct ±¸Á¶´Â intact·Î ³²À½.

Slight interstitial fibrosis¿Í fat necrosis°¡ ÀÖ´Ù.

¿©·¯°¡Áö °æ¿ì¿¡ ÀÖ¾î ¿°ÁõÀÌ Àç¹ßÇϱ⵵ Çϰí ÀÚ¿¬Ä¡À¯ °æÇâÀÌ ÀÖ´Ù.

遁. Hemorrhagic ÃéÀå¿°

; ÃéÀå ½ÇÁú ÆÄ±« ¹× ÀÀ°í¼º ±«»ç

Ãʱ⿡´Â ¹éÇ÷±¸ ħÀ±ÀÌ spareÇϳª ³ªÁß¿¡´Â plentiful

½ÇÁú Ç÷°üÀº ±«»çµÇ°í ±×°á°ú ¸¹Àº ºÎÀ§ÀÇ ÃéÀå ÃâÇ÷ÀÌ ÀÖ´Ù.

` Áö¹æ ±«»ç´Â ¹Ì¸¸¼ºÀ̰í ÃéÀå °áÇÕÁ¶Á÷¼º °Ýº®, ÃéÀåÁÖÀ§ Áö¹æÁ¶Á÷,

º¹°­³» Áö¹æÁ¶Á÷, º¹°­¹ÛÀÇ Áö¹æÁ¶Á÷±îÁö ÀϾ

` ¼±Á¶Á÷Àº ½ÇÁúÁ¶Á÷ÀÇ ÆÄ±«¿¡ ÀÇÇØ grayish-white mottled µÇ°í,

Chalky-white deposits°¡ fat necrosisµÈ ºÎÀ§¿¡¼­ µÇ°í

; friable, soft, red areas´Â bleeding¿¡ ÀÇÇÑ Á¶Á÷ÆÄ±«¸¦ ¾Ï½Ã

Causes

; Obstruction of the pancretic duct, Diatery factor, Infectious agent,

Trauma, Toxic drug reaction, Metabolic abnormalities, Vascular alterations


1. Pancreatic Duct Obstruction

- ½ÇÇèÀûÀ¸·Î Æó»ö½Ã۸é hypersecreation Çϳª ÀÚ¿¬ÀûÀÎ °æ¿ì´Â µå¹°´Ù.

- Ãé°ü°ý¾à±ÙÀÇ ºÎÁ¾À̳ª °æ·Ã, Morphine, ½ÊÀÌÁöÀåÀÇ ºÎÁ¾À̳ª Á¶¾ç¿¡ ÀÇÇØ

- Æó»öãÁ Golgiô÷·Î ÃéÀå È¿¼Ò ÇÕ¼º°ú ¼ö¼ÛÀº Á¤»óÀ̳ª, ¼ÒÈ­È¿¼Ò ºÐºñ°¡ Â÷´ÜµÊ

- Large vacuoles ³»¿¡ ¼ÒÈ­È¿¼ÒµéÀÌ °üÂûµÊ.

- ColocalizationÀÌ ¼ÒÈ­È¿¼ÒȰ¼º°ú ¼±¹æ³»·Î ºÐºñ¸¦ ÀÏÀ¸ÄÑ Autodigestion°ú

Ȱ¼º ProteaseÝÂÝô¸¦ ÃËÁø ½ÃÅ´.

2. Diatary factors

- °³°¡ Åë»ó obeseÇÏ´Ù.

- High fat diet ( ÃéÀå ¼±¹æ¼¼Æ÷Ò® ¼¼Æ÷¸·ÀÇ Åõ°ú¼º °áÇÔ À¯µµ·Î ¼Õ»ó°ú

autodigestionÀ» À¯¹ß) À» Àå±â°£ Åõ¿© ãÁ.

3. Infectious Agents

- Viral or Parasitic infection, Bacterial infection Àº rare.( º¸°í´Â ÀÖÀ¸³ª

È®ÁõÀº ¾ø´Ù.)

Ç㳪 BacteriaÀÇ °æ¿ì severity¸¦ Áõ°¡ ½ÃÅ´.

4. Trauma

- Accidental or Surgical trauma - blunt abdominal trauma.

- Surgical manipulation in this area (ぢ Bile ductっ ¼ö¼ú½Ã )

5. Drug

- Azathioprine, Thiazide, Sulfonamide, Furosemide,, Estogen, Tetracycline,

Metronidazole, Gluococorticoids

6. Metabolic Disorders

- Hyperlipidemia, Hypercalcemia,(HypertrtriglycemiaÀÇ ±âÀüÀº ºÒÅõ¸í )´Â

°³¿¡¼­ Acute pancreatitis¿Í °ü·Ã ÀÖ´Ù.

- FFA( free fat acid; ÃéÀå LipaseÀÇ Áõ°¡¿¡ ÀÇÇØ)´Â toxic concerationÀÇ Áõ°¡

=>¿°Áõº¯È­¸¦ À¯µµÇϰí Maniature schnazerÀÇ °æ¿ì Idiopathic

Hyperlipoproteinemia¿Í °ü·Ã

- Ca++³óµµ¸¦ Áõ°¡ ½ÃŰ´Â ¿äÀεé ( Hyperparathyroidism,Acute pancreatitis )

; Ca++ ³óµµ »ó½Â => ÃéÀå ºÐºñ Áõ°¡ => trypsinogen Ȱ¼º Áõ°¡ => Proteolytic

cascade¿Í trypsin, chimotrypsinogen, propholipase A, Lipase¸¦

Stabilation½ÃÄѹö¸².

7. Vascular Alterations

- Thromboembolism, vasculitis, severe hypotensionÀÌ ¿øÀÎ

- ÃéÀåÀº ¸Æ°ü ȯ·ù º¯È­¿¡ ¹Î°¨ÇÑ Àå±â¿©¼­ DIC ( Disseminated Interavascular

Coagulation) °¡ ÀϾ±â ½±°í , ÇãÇ÷¿¡ ÀÇÇÑ Á¶Á÷±«»ç°¡ pancreatic proteaseÀÇ

Ȱ¼º¿¡ °ü¿© ÇÑ´Ù°í º½.

PATHOPHYSIOLOGY

* AntiproteaseÈ¿°ú¸¦ ¹æ¾î ÇÒ¼ö ÀÖ´Â ±âÀüÀ» ÆÄ±« ÇÏ´Â °Í ;

衁. ¼¼Æ÷´ë»çÀÇ Â÷´Ü.

遁. ¼±¹æ¼¼Æ÷³» lysosomal hydrolases ÁÖÀ§ÀÇ ¼¼Æ÷¼º lipoprtein¸·ÀÇ Åõ°ú¼º Áõ°¡

鑁. ºÎÀûÀýÇÑ proenzyme Ȱ¼º°ú autodigestion

* ÃéÀå¿¡ ´ëÇÑ ÃéÀåÈ¿¼Ò¿Í È¿°ú

- TrypsinÀÇ activators ( Enterokinase, cathepsin B, low pH )

Biochemical Effect ( Proteolysis, activation of proenzymes )

Predominant Histologic Effect onthe Pancreas( ºÎÁ¾,¾×È­±«»ç,ÃâÇ÷)

- Chymotrypsin -> Trypsin

-> Proteolysis

-> ºÎÁ¾, ÃâÇ÷

- Elastase -> Trypsin

-> Blood vessel elastolysis

-> ÃâÇ÷

- Phospholipase A -> Trypsin, Bile acids

-> Formation of lysophosphatides

-> Coagulation necrosis, Fat necrosis

- Lipase -> Bile acids

-> Triglycerides ¸¦ ºÐÇØ

-> Fat necrosis

* Proenzyme activation, Pancreatic elastase, Phospholipase A ´Â

-> ÀÀ°í¼º ±«»ç,vascular injury ( elastolysis, ÃâÇ÷, Ç÷Àü )À» Ç×Áø.

-> glossy edema, enzyme rich fluid ÝÂÝô, pain À¯µµ.

* Pancreatic proteases -> ÃéÀå °£±ØÀ¸·Î -> º¹¼ö¾×°ú Ç÷ûÀ¸·Î

-> alpha-macroglobulin, alpha-antitrypsin, proenzymes ÇüÅ·Πº¹±¸

-> protease inhibitorÀÇ imbalance À¯µµ

-> ÃéÀå¿°À» ¾ÇÈ­, ´õ³ª°¡ º¸Ã¼, Kinin,ÀÀ°í ¹× ¼¶À¯¼Ò ¿ëÇØ°èÀÇ È°¼º.

-> ÃéÀå ¹Ì¼¼ Ç÷°ü°è ÇãÇ÷¼º ÀåÇØ¿¡ ÀÇÇØ ºÎÁ¾¹× ±«»ç.

-> ÀúÇ÷¾Ð À¯µµ -> Death

-> Cardiac index Áõ°¡, ¸Æ°ü ÀúÇ×¼º ÀúÇÏ

DIAGNOSIS

* WBC Áõ°¡, Ç÷¾× ³óÃà, ºóÇ÷, Azothemia, { ÊÜ È¿¼Ò,ºô¸®·çºó Áõ°¡ },

Ç÷´ç Áõ°¡, Ca++ ³óµµ °¨¼Ò, Ç÷Áö¹æÁõ, Na+ ³óµµ°¡ ³ô°Å³ª ³·°Å³ª, K+ ÀÇ Áõ°¡.

* Middle-aged, old Dog ÀÌ °©ÀÛ½º·´°Ô depression Çϰí, vomittingÇϰí anorexia°¡

¿À¸é ÀǽÉ.

1. History ¿Í ÀÓ»ó Áõ»ó

ÈçÈ÷ º´¹ß; middle aged, old, obase, female dog ( Á¤»ó BWÀÇ Male¿ª½Ã )

Vomitus ; partially digested food, ÈÄ¿¡ bile & watery mucus·Î ±¸¼ºµÊ

óÀ½ ±¸ÅäÈÄ¿¡ °è¼Ó regurgiative motion ¸¸ º¸ÀÓ.

Posture´Â Á¤»óÀ§, upright with abdominal tucking, lateral recumbency

( painÀ̳ª ÀúÇ÷·®Áõ½Ã )

Diarrhea ; °¡²û, scant, abscent feces°¡ ´õ ÈçÇÔ ( º¹¸· ¿°·ù·Î ilus )

* Physical Examination

- mild depression, normal vital sign, Á¤»ó º¹ºÎ tenderness ( mild °æ¿ì )

- Hemorrhagic case ; marked depression, fever, hypotension, tachtpnea,

weak femoral pulse, painful abdomen,

moderate to maked dehydration.

* ÀÓ»óÀûÀ¸·Î icterus´Â °¨Áö µÇÁö ¾ÊÀ¸³ª cholestasis¿¡ ÀÇÇØ¼­ °üÂûµÈ´Ù.

- Bile duct´Â rare, º¹ºÎ È®ÀåÀº paralytic ileus

- Reddish - Brown ascitic fluid°¡ ÃâÇ÷¼º ÃéÀå¿°ãÁ °üÂû

- Ãʱ⿡ °¨º° Áø´Ü ÇØ¾ß ÇÒ °Í

±Þ¼º À§Àå¿° , Áßµ¶, blunt abdominal trauma , À§Àå°ü Æó»ö , À§Àå°ü õ°ø

Àå°ü Volvulus , Àå°ü ÇãÇ÷°ú °æ»ö , ±âÁ¾¼º ´ã³¶¿° , Ruptureed organ,

±Þ¼º ½ÅºÎÀü , ±Þ¼º °£Áõ .

; ÀÌ·¯ÇÑ ±Þ¼º º¹ºÎ ÁúȯÀ¸·Î¼­ pancreatitis ¿Í ½Å¼ÓÈ÷ °¨º°Çϱâ À§ÇØ

X-ray, BUN, GPT, GOT ÃøÁ¤À» ÇÑ´Ù.

2. Radiographic Findings

- Mild edematous pancreatitis

- Stomach¿Í Duodenum¿¡ normal to mild ileus.

- More severe case (º¹¸·¿°¿¡ ÀÇÇØ ) ; îñÜÙÝ»´Â ³»ÀåºÎÀ§´Â Film¿¡¼­

DetealÀÌ ¼Ò½Ç.( Fluid density°¡ Áõ°¡ µÇ¾î¼­)

- Right-sided lateral displacement of gas-distend duodenum &

gastric distention

- Pleural effusionÀ̳ª pulmonary fluid accumulation.

3. Clinicopathologic Findings

- Serum amylase test ( amyloclastic method needed ) ; 2 ~ 3¹è Áõ°¡´Â

½Å±â´É ºÎÀü°ú ±Þ¼º ÃéÀå¿°ãÁ

- Serum lipase ( ´õ Á¤È®ÇÔ ) ; Hepathic, renal, Á¾¾ç¼º ÁúȯãÁ.

TREATMENT

1. Medical Therapy

- Oral food intake restriction ( Normal hydration À¯Áö¸¦ À§ÇÑ fluid

°ø±Þ¸¸ ÇÑ´Ù.)

- Indwelling venous cather »ðÀÔ

- Relive pain ( if severe)

- AntibioticsÅõ¿©

- ü¾× º¸Ãæ

- Insulin Åõ¿© ( ÀûÀýÈ÷ )

a. Food restriction

* ´ÜÁö Àǽɸ¸ µÇ´Â °æ¿ì ; Áø´Ü µÉ¶§ ±îÁö ¹°¸¸ ¸ÔÀ̸鼭 1 ~ 2 ÀÏ ±¾±è.

VomittingÀÌ Áö¼ÓµÇ¸é, 5 ~ 7 ìí ÀÌ»ó ( ½ÉÇÑ °æ¿ì 2ÁÖ ±îÁö )

|-> ü¾×º¸Ãæµµ IV ·Î

b. Fluid Replacement

- °¡Àå Áß¿ä

- Marked hypotension ãÁ ; ºü¸£°Ô º¸ÃæÇϸç, lactated Ringer or Saline À»

30 ~ 40 ml During 1 ~ 2 hrs,

Vital signÀÌ Á¤»óÈ­µÇ°í ¿ä¹è¼³ÀÌ ÀûÀýÇÏ°Ô µÇ¸é

À¯Áö·®À» 15 ~ 25 ml/kg, 22 ~ 23 hrs

* Maintenance Sol. { 2.5 ~ 5 % Dextrose , 0.45 % Saline with

KCl ( 3 ~ 5 mEq/kg/day ) + Vit B complex. }

衁.Acid - base balanceÀ» ¸ÂÃß°í

遁.HypoproteinemicãÁ ( albuminÀÌ 2.3 g/ dl ÀÌÇÏ ) - fresh plasma°ø±Þ

=> ºÎÁ¾ ¹æÁö, ½ÅºÎÀü ¹æÁö, »ïÃâ ( ³»Àå ) ¹æÁö, pancreatic protease·Î

¿ªÈ° ( Dextran °°Àº Colloidal Sol. ÀÌ¿ë ʦÒö )

鑁. urine out-put¸¦ °üÂû ( ü¾× ±³Á¤ÈÄ¿¡ )

鱁. Oliguria ³ª anuriaãÁ furosemid·Î diuresis ¸¦ À¯µµ Çϰí, »ïÅõ¼º

ÀÌ´¢Á¦´Â ÀÌ¹Ì hyperosmoralityÀ̹ǷΠ±Ý±â.

ꁁ. ü¾× À¯Áö·® = ¿ä¹è¼³¾ç + ü¾× ¼Õ½Ç¾ç

Anuria ±â°£¿¡ °­Á¦·Î ü¾× ÀÌ´¢¸¦ ½ÃŰ´Ù°¡ Ä¡»çÀûÀÎ ÆóºÎÁ¾ À¯¹ß.

c. Parasympatholytics´Â ( atropin °°Àº ) side effect°¡ °­Çؼ­ ÞÅéÄ ÝÕʦ.

- Antiemetics ( metoclopramide hydrochloride ) ºÎ±³°¨ ½Å°æ ÈïºÐ È¿°ú ¾øÀÌ

»ç¿ë. 0.2 ~ 0.4mg/kg, SC, 16 ~ 18 hrs. or 1mg/kg, day, IVãÁ

- Cimetidine ( À§»ê ºÐºñ ¾ïÁ¦ È¿°ú ) - ÀÌ·ÐÀûÀÎ °ÍÀÓ

- Antibiotics ( morderate to severe case ¶§ »ç¿ë )

Septicemia, ¿ä·Î°¨¿°, Æó·Å, ÃéÀå³ó¾çÀÌ ½±°Ô µÇ¹Ç·Î antibiotics´Â

Broad spectrum¿¡ aerobic & anaerobic À» °í·ÁÇÏ¿© Åõ¿©.

ÁÖ·Î Ampicilline, CM, Cephalothin À» ¾ÈÀüÇÏ°Ô Åõ¿©.

Aminoglycoside´Â ½Åµ¶¼ºÀÌ ÀÖÀ¸¹Ç·Î ÁÖÀǸ¦ ¿äÇÔ.

d. ¿µ¾ç°ø±Þ

°¡Àå ¾î·Á¿îÁ¡À̹ǷÎ

- 5% Dextrose·Î ¸îÀϰ£Àº °¡´É Çϳª, ÀÏÁÖÀÏ ÀÌ»ó ±Þ½ÄÀ» Á¦ÇÑÇÑ °æ¿ì

Calorie ¿ä±¸¸¦ ¸ÂÃ߱Ⱑ Èûµë.

- º¸Åë 5 ~ 7 ìíÈÄ¿¡ Liquid diet ·Î Àç±Þ½ÄÈÄ Solidsàõ À½½ÄÀ¸·Î ¹Ù²Ù¾î °£´Ù.

VomitingÀÌ ÀÖÀ¸¸é IV·Î ÇÒ ¼ö ¹Û¿¡.

- IV·Î ¾Æ¹Ì³ë»ê°ú Áö¹æ»êÀÌ °ø±ÞµÇ¸é ÃéÀå ºÐºñ¸¦ ÀÚ±ØÇÏ°Ô µÈ´Ù.


* Àå±â°£ IV °ø±ÞãÁ ¹®Á¦Á¡

衁. Ä«Å×ÅÍ¿¡ ÀÇÇÑ Á¤¸Æ¿°

遁. ÆÐÇ÷Áõ

鑁. Ç÷Àå °í»ïÅõ¼º

鱁. ±î´Ù·Î¿î Áغñ¿Í µ·.

- Tube jejunostomy °¡´É

e. µ¿Åë ±¸Á¦

- Phenothiazine ( ±Ý±â - ÀúÇ÷¾ÐÀ» ¾ÇÈ­ ½ÃÅ´ )

- Meperidine HCl ( 5 ~ 10 mg/kg, preferred )

f. Insulin

- ÀϽÃÀû ÀÛ¿ë ; Ç÷´çÀÌ 300 mg/dl ÀÌ»óãÁ Crystalline zinc insulin ( 0.5 U/kg )

- Áö¼ÓÀû ÀÛ¿ë ; ´ç´¢º´ Ä¡·á¿¡ ÁØÇؼ­

TABLE 11

Clinicopathologic Abnormalities Accompanying Acute Pancreatitis in Dog

Abnormality | Proposed Mechanism

-------------------------------------------------------------------------------

Leukocytosis | Inflammation,stress, hemoconcentration, secondary infection

Hemoconcentration | Dehydration,translocation of plasma into abdominal cavity

Anemia | Hemorrhagic abdominal effusion, iatrogenic crystalloid

fluid effusion

Azotemia | Prerenal from dehydration, renal from hypovolemia or

disseminated intravascular coagulation; idiopathic renal failure

Liver enzymes and | Focalhepathic necrosis, hepatic lipidosis,

bilirubin cholangiohepatitis, cholangiostasis

Hyperglycemia | Elevated stress hormones ( growth hormones, glucorticoids,

glucagon, epinephrine ), hypoinsulinemia, destruction of

islet beta cells

Hypocalcemia | Calcium-soap formation ( the most widely accepted

mechanism)

Hyperlipidermia | Might preexist as a separate entiy; can occur with

pancreatitis, but exact mechanism is unknown ; possibly

related to release of stress hormones( GH, glucocorticoids,

glucagon, epinephrine )

Hypernatremia | Dehydration

Hyponatremia | Vomiting, psedohyponatremia from hyperlipidemia

Hypokalemia | Vomiting, failure to supplement parenteral fluids,

osmotic diuresis from hyperglycemia

Hyperamylasemia & | Direct venous absorption of enzymes from the inflamed

hyperlipasemia pancreas & absorption via transperitoneal lymphatics &

lymphatic drainage from the pancreas & surrounding tissue

* Yorkie ¹Ì¿ë

¹ßÀ» µ¤À»°Í, ±Í´Â 2/3 Á¤µµ ( ¸Ó¸®°áÀ» µû¶ó )

ÅÐÀº cut °¡À§·Î °áÀ» µé¾î ÀÚ¸¥´Ù

Ç×¹®ÅÐÀº °¡À§·Î ÀÚ¸£°í, ´Ù¸®´Â °Å²Ù·Î ºø¾î¼­ ÀÚ¸¥´Ù.