- 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.
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×ȱ«»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°¸¸ ¸ÔÀÌ¸é¼ 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.