Acute Bleeding And Acute Abdomen And Peritonitis Flashcards

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1
Q

State some causes of acute bleeding

A

IATROGENIC
•TRAUMATIC/INJURIES – FRACTURES, OPEN/STAB WOUNDS, G.I/ PERFORATIONS (VISCOUS), VASC. RUPTURE, EXPLOSIONS, ETC
•HAEMATOLOGICAL – DIC, HAEMOPHILIA, SCD, EMBOLI, ETC
•GYNAECOLOGICAL/OBSTETRICS.
•NEOPLASTIC – BRAIN TUMOR, COLON/ LUNG/ BREAST CAs, ETC
•INTRACRANIAL - CVA, RUPTURED ANEURYSMS, OTHERS
•DRUGS.
•OTHERS.

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2
Q

Pathophysiology of bleeding depends on what?

A

THE MECHANISM OF INJURY TO THE VASCULATURES
•THE BODY’S RESPONSE TO THE INJURY - VIRCHOW’S TRIAD
•THE VOLUME OF BLOOD LOSS

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3
Q

the types of bleeding are based on what things?

A

THE VASCULAR –ARTERIAL, VENOUS AND CAPILLARY.
THE BODY LOCATION – INTERNALLY AND EXTERNALLY.
THE VOLUME OF BLOOD LOSS – MINOR AND MAJOR.
THE DURATION – ACUTE AND CHRONIC.

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4
Q

What is shock

A

Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization.

  • Inadequate oxygen delivery to meet metabolic demands
  • Usually results from global tissue hypoperfusion and results in metabolic acidosis

•Shock can occur with a normal blood pressure and hypotension can occur without shock

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5
Q

State the types of shock

What are the types of hypovolemic shock and give examples under each

A
Hypovolemic
•Cardiogenic
•Septic  
•Anaphylactic
•Neurogenic
•Obstructive
Hemorrhagic
•Trauma
•GI Bleed
•Massive Hemoptysis
•AAA rupture
•Ectopic pregnancy or Post-partum bleeding
•Non-hemorrhagic
•Vomiting/Diarrhea (Gastroenteritis)
•Small and Large Bowel obstruction
•Pancreatitis
•Burns
•Environmental (Dehydration)
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6
Q

Cardiac output is equal to what?
Blood pressure is equal to what?
What is stroke volume?
Stroke volume is a function of what factors

A

Cardiac Output = SV X HR

Thus,

Blood Pressure = SV X HR X PVR

Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance

Stroke Volume = Volume of blood pumped by the heart during 1 cardiac cycle
10

Stroke Volume is a function of what factors?
Myocardial contractility
Preload
Afterload

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7
Q

What is the pathophysiology of shock

A
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8
Q

What is the physiologic compensation in shock

A

Heart rate increases as a compensatory response to Shock
•Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery
–Sympathetic nervous system
•NE, epinephrine, dopamine, and cortisol release
–Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output)
–Renin-angiotensin axis
•Water and sodium conservation and vasoconstriction
•Increase in blood volume and blood pressure
•Goal is to maintain cerebral and cardiac perfusion
–Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow

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9
Q

What is multi organ dysfunction syndrome

What is the clinical presentation of someone with this?(history and physical exam)

A

Inability of O2 to meet metabolic demands despite attempts at physiological compensation leads to triad of lactic acidosis, cardiovascular insufficiency and increased metabolic demands
•Downward spiral continues with progression of physiologic effects:
–Cardiac depression
–Respiratory distress
–Renal failure
–Disseminated Intravascular Coagulation (DIC)
•Result is end organ failure and death

History
–Recent illness/Trauma
–Fever
–Chest pain, SOB
–Abdominal pain
–Co-morbidities
–Medications
–Toxins/Ingestions
–Recent hospitalization or surgery
–Baseline mental status
Physical examination
•Vital Signs
•CNS – mental status
•Skin – color, temp, rashes, sores
•CV – JVD, heart sounds
•Resp – lung sounds, RR, oxygen sat, ABG
•GI – abd pain, rigidity, guarding, rebound
•Renal – urine output
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10
Q

What are the diagnostic tools used in MODS

A
Diagnostic Tools
•Physical exam
•Clinical signs and symptoms vary depending on the severity of disease and early recognition is key to diagnosis and intervention
•Basic Labs:
•CBC
•Chemistries
•Lactate
•Coagulation studies
•ABG
•Blood cultures (septic screen)

Additional Diagnostic Tools
•CT of head/sinuses for occult infections/abscesses
•Lumbar puncture for meningitis/encephalitis
•Wound cultures
•Acute abdominal series
•Abdominal/pelvic CT or US
•Fibrinogen, FDPs, D-dimer if suspicion for DIC is high

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11
Q

What’s the initial approach to shock?

A
ABCs
•Cardiorespiratory monitoring
•Pulse Oximetry
•Supplemental oxygen
•Large bore IV access x 2
•ABG, labs
•Foley catheter
•Vital signs including rectal temperature (core temparature)
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12
Q

How do you estimate blood pressure in a shock patient

How is hypovolemic shock classifies

A

Quick method of estimating the blood pressure in patients
•If you palpate a pulse in these regions, then you know the SBP is at least this number:
60 in the arms
80 in the groin
90 in the knees

CLASS I - IV
•BVL - < 15%, 15 - 30%, 30 - 40%, > 40%
•AMOUNT - 750 cc, 750 - 1500 cc, 1500 - 2000 cc, > 2000 cc
•PULSE – <100, >100, >120, >140
•BP
•RESP
•CNS
•Urine
•TX
                   REFER TO TABLE.
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13
Q

What is the hypovolemic shock threatment goals

A

ABCDE
•Airway: Assess airway patency and intervene in critically ill patients to decrease work of breathing and support airway control
•Intubation and mechanical ventilation can initially worsen hypotension
•Sedatives can lower blood pressure
•Positive pressure ventilation decreases preload
•May need aggressive volume resuscitation prior to intubation to prevent hemodynamic collapse

•Control work of Breathing: Respiratory rate increases with shock to compensate for metabolic acidosis
•Respiratory muscles consume a significant amount of oxygen
•Tachypnea can further exacerbate lactic acidosis
•Mechanical ventilation and sedation will decrease work of breathing and improve overall survival
•Optimize Circulation: Isotonic crystalloids (Normal Saline or Lactated Ringers) is optimal first-line fluid
•Titrate to:
•CVP 8-12 mm Hg if you have central venous access
•Maintain urine output 0.5 – 1.0 ml/kg/hr (30 ml/hr)
•Improve heart rate (Goal HR < 100)
•Often requires large amounts of fluids or blood products (>4-6 Liters)
•No survival or outcome benefit from colloids
•Adequate oxygen Delivery: Decrease oxygen demand for patients
–Provide analgesia and anxiolytics to relax muscles**
–Avoid shivering
•Maintain and increase arterial oxygen saturation
–Give supplemental oxygen
–Maintain hemoglobin > 7 g/dL
•Tissue oxygen extraction can be measured with serial lactate levels on an ABG or central venous oxygen saturations if equipment is available
•Monitor End points of resuscitation:

Use objective hemodynamic and physiologic parameters to guide specific therapy
–i.e. Check vital signs and physiologic markers frequently

•Directed parameters to follow
–Urine output > 0.5 mL/kg/hr (simplest measure)
–CVP 8-12 mmHg (if central venous access available)
–MAP 65 to 90 mmHg
–Central venous oxygen concentration > 70% (if central venous access available)

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14
Q

How is hypovolemic shock managed

A

ABCs, IV/O2/Monitor
•Establish 2 large bore IVs or a central line
•Crystalloids
•Normal Saline or Lactate Ringers
•Up to 3 liters in adults
•Pediatrics = 20 cc/kg boluses (may need multiple boluses)
•Blood Products (Whole Blood, PRBC’s/FFP/Platelets)
•O negative or cross matched if type specific is not available
•Control any sources of active bleeding
•Arrange definitive intervention for hemorrhagic shock (Operating Theatre)

Hypovolemic Shock
•Evaluate response to treatment

A. Rapid Response
B. Transient Response
C. No Response

Based on
•Vitals - return to normal, Transient improvement with return to previous, Remain Abnormal.
•Estimated Blood loss- 10-20%, 20-40% with ongoing likely, Severe >40%.
•Need for more Fluid - Low, High, High.
•Need for Blood - Type and cross, type specific, O-Neg.
•Need for surgery - Possible, likely, highly likely

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15
Q

What is peritonitis
Depending on the underlying cause, the result is
What are the classes of peritonitis and define them

A

Inflammation of the serosal membrane or the lining of the abdominal cavity and its content
Depending on the underlying cause, the result is
•Infectious
•sterile- chemical

Introduction of infection – into a sterile environment

•Irritantants- HCL, Bile, foreign bodies and blood

Primary- from haematoginous spread – young 1 to 10year in older persons – cirrhosis and ascites. Nephrotic syndrome

  • Secondary – from inflammation of organs, perforations etc.
  • Tertiary- persistent or recurrent infection after adequate initial therapy.
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16
Q

Secondary peritonitis may be what or what
What type of peritonitis is the most common
Organisms from the upper gi are predominantly what type and the lower GI are what type
State the causes of secondary peritonitis
Name two iatrogenic causes

A

Secondary peritonitis may be
I. localized
II. generalized

Secondary Peritonitis

  • most common form of peritonitis
  • Mostly they are polymicrobial when cultured

Organism from Upper GI are predominantly G-pos

•Lower GI mixture of anaerobic and G–neg aerobic microbes.

causes

  1. Appendicitis
  2. Perforating peptic ulcer,
  3. Diverticulitis ,
  4. Vulvulus / perforation
  5. Perforations of other organs(typhoid perf).
  6. Neoplasms of colon
  7. Penetrating trauma

Iatrogenic causes.
I. Instrumentation and operation of organs.
II. Anastomotic leaks

Ischaemia and gangrene of bowel

  • Salpingitis, salpingo-oophritis
  • Pyelonepheritis , complicated cholecystitis
  • Inflammatory bowel disease.
17
Q

When does primary peritonitis occur
Exclusively occurs in which patient
How does it happen

The majority of primary peritonitis are monomicrobial- 90%

•Multiple isolates are found in less than 10%
True or false

What are the most frequent organisms in primary peritonitis

A

Occurs in the absence of an apparent intra-abdominal source of infection

  • Exclusively occur in cirrhotic patient.
  • Less frequently – young girls and boys

How does it happen?

  • Translocation through the wall of ischaemic bowel or mesenteric lymphatic
  • Or via a haematogenic spread to the peritoneum
  • Incidences tend to increase with the concentration of protein of the ascitic fluid.

Antibiogram
•Most frequent organisms are G-neg – e-coli 40% Klepsiella -pneumonae 7% Pseudomonas spps, Proteus and other G-neg species (20%).

  • less frequently G-Pos Strep pneumonae 15%
  • Other Streptococcus species 15% Staphylococcus species 3%
18
Q

What is tertiary peritonitis
Patients w this usually present with what?

Normally the original visceral pathology is no more present true or false
This kind of peritonitis is associated with what?
Which organisms are normally isolated ?

Antibiotic are less effective

  • Poor localization of abscesses
  • Frequently need surgery and relook operations to get source control.

•High Mortality- 70%
True or false

A

Tertiary peritonitis represents as persistent or recurrence of peritoneal infection following apparently adequate therapy for primary or secondary peritonitis

Patients with tertiary peritonitis usually present with an abscess, with or without fistulization

They are associated with a longer length of stay in the hospital .

  • Worse prognosis
  • Mortality of 50% to 70%
  • Organisms Isolated normally of resistant strains and unusual (eg, Enterococcus, Candida, Staphylococcus, Enterobacter, Pseudomonas species)
19
Q
TB peritonitis is increasingly become frequent in which countries and increases with what infestation
More common in which patients
What’s re the presenting symptoms 
Fluids may have what components?
There is laporoscopic evidence of what?
Chest X ray shows what
A

Increasingly becoming frequent in developing countries

  • Increasing with increasing HIV infestation.
  • More common in patients with liver cirrhosis, and those with asciitis
  • Presenting symptoms are insidious – low-grade fever, anorexia, weight loss

Cultures of the peritonial fluid are frequently falsely negative
•Fluid have a high protein content > 2.5g/dl
•LDH level > 90 U/mL.
•Laparoscopic evidence of granulomatous lesions.
•Chest X-ray may also show evidence of pulmonary disease-yet this is uncommon. Occurring in <30%.

20
Q

Chemical peritonitis is caused by what
Overall effect of bacterial peritonitis depends on what?
In pathophysiology what happens

A

Chemical peritonitis – are caused by irritants.
bile, blood and barium

Bacterial peritonitis generates a significant local and systemic response.

Overall effect is dependent on

  1. the virulence of the contaminant,
  2. the size of the innoculum
  3. the immune status and overall health of the host

The large peritoneal surface area, its semi permeable character and absorptive capacity couples with vascular permeability results in absorption of toxins and bacterial access to blood
•Bacteremia
•Sepsis
•Septic shock.

Peritonial inflammation – results in a slugging intestinal activity – leading to a paralitic ileus

  • Due to an impaired myenteric activity
  • Worsening fluid sequestration and yet limits bacterial spread.

Resulting shock – initially compensated, yet it may lead to eventual circulatory collapse

  • Abdominal distention negatively affects respiratory active
  • microbiology event and endotoxic triggers lead to the initiation of a process that could lead to ARDS

•Shock negatively impacts on renal function. –pre-renal failure, etc.

21
Q

What are the clinical features of peritonitis

A

Pain- may start locally, becoming generalized depending of the primary cause

  • In chemical peritonitis inflammatory is significant and fast leading to a board like rigidity.
  • Generalized diffuse pain which is constant worsened by breathing and moving
Nausea
•Vomiting
•Anorexia
•Constipation
•Diarrhoea
•Oliguria
•Fever and  chill
22
Q

What is acute abdomen
Surgical abdomen shows what
Name three characteristics of surgical abdomen

A

Sudden onset of severe abdominal pain, significant enough to warrant seeking medical attention and which MAY require a surgical intervention.

•Surgical abdomen shows evidence of peritoneal inflammation- peritonitis

Several factors make a quick evaluation and diagnosis critical to achieving optimum outcome.

I.Surgical abdomen require an intervention
II.They deteriorate rather fast
III.Outcome worsen with time

23
Q

What is the history of someone w acute abdomen

How will you characterize the pain using SOcRaTes and how will you evaluate the pain using the PQRST

A

Key to unraveling the cause of the acute abdomen
•Detailed, systematic and accurate history
•Properly evaluating the main complaint – PAIN
•Medical, Surgical and Gynaecologic history
•Social history

PAIN – main complain.

•Location – epigastric
umbilical
hypogastric/ suprapubic
back

•Character visceral
somatic

Dull continues, colicky and frequent or occuring in paroxysms  - as in biliary colics

The classic PQRST mnemonic for a complete pain history is as follows:
•P3 – Positional, palliating and provoking factors
•Q – Quality
•R3 – Region, radiation, referral
•S – Severity
•T3 – Temporal factors (time and mode of onset, progression, previous episodes)

24
Q

What factors may make acute abdominal pain seem less acute

Explain onset as a characteristic of acute abdominal pain

A
Factors that may make pain seem less acute
•Age
•Autonomic neuropathy
•DM
•Paralysis
•Steriods

Sudden is a sign of impending catastrophy

  1. Messenteric ishchemia
  2. Vulvulous
  3. Tortioning/ ischeamia of internal organ
  4. Perforated viscus- perf. DU or gastric
25
Q

Explain referred pain as a characteristic of acute abdominal pain
State four other aspects of pain evaluation

A

Referred pain may indicate the location of a pathology

Diaphragmatic irritation – shoulder tip pain –kher sign

Pain radiation to the inter scapular area / referred pain right scapular—related to inflamed gall bladder.

Duration of pain

  • Progression of the pain
  • Relieving and aggravating factors

•History of recurrent episode may point to a medical cause.
Intensity of pain

26
Q

Explain associated symptoms as a characteristic of acute abdominal pain
State bowel symptoms seen in acute abdominal oain and what they show

A

Anorexia

  • Vomiting -
  • content
  • bilious non bilious
  • feaculent
  • Projectile
  • effortless or non productive
  • Haematemesis ( coffee grounds)

•Self limiting vomiting may be related to a medical condition

Bowel symptoms
•Diarrhoea – don’t be comforted by its presence

  • Inability to pass of flatus is a more reliable symptom than constipation
  • Bloody stools in acute abdomen may point to a mucosal ischaemia

Melaena stool
•Haematochezia
•Urge to defecate with severe abdominal pain – ectopic pregnancy , raptured aneurysm in older patients

27
Q

State genitourinary l symptoms seen in or may cause acute abdominal pain

A

Genitourinary symptom may be associated with, or may be the cause of the acute abdominal pain
•Testicular torsion may appear abdominal initially
•An enlargening uterus may confound symptoms associate with an acute abodomen

28
Q

State diseases seen in or that may cause acute abdominal pain

A

Cardiopulmonary symptoms
•Syncopal attacks
•Pneumonia
•Pulmonary embolism

MI
•DKA
•Gastro enteritis
•Hypercalcaemia
•Addison's disease
•SCD ( sickle cell disease)
•Porphyria ( Acute Intermittent Porphyria)
29
Q

What drugs can cause acute abdominal pain

What shouod you focus on in social history t

A

Use if NSAIDS
•Immunosuppressive agents
•Use of narcotic drugs

Alcohol
•Smoking
•Recreational drug use

30
Q

What exam findings can you see in acute abdominal pain

Explain cullens signs and Gray Turners signs

A

ill looking
•Lying still or restless
•Abdomen may move with respiration or held still
•May look distended
•Sweating or look dehydrated with sunken eyes

•May feel warm to touch

Examination
•Tenderness
•Rebound tenderness
•Guarding (involuntary) rigidity/ or voluntary guarding.
•Heel strike
  • Abdominal distention
  • Auscultation – increased or reduced bowel sounds. Bruits

Rectal examination

Cullen’s sign- discol. of the umbil. area due intraperito. hemorrh. from any cause.
•Gray Turner’s sign – inflamm. of the left flank ass. with acute hemorrh. pancreatitis

31
Q

Which sign has the highest sensitivity between Murphys, Rovsing’s sign ,cough sign
State five investigations for acute abdomen

A

Murphys sign 67% sensitivity

  • Rovsing’s sign low sensitivity (15-35%) specificity (85-95%)
  • Cough sign – Rostovzev (1909) Benette and colleagues – 78% sensitivity and 79%specifity
  • Psoas sign-
FBC
•BUE
•CMP
•LFT’s,
•Amylase, lipase
•ABG + lactate  
•Pregnancy
32
Q

State four ddx each of the abdominal pain by the four quadrants and Epigastric site

A

RUQ– cholecystitis, PUD, gastritis, pancreatitis, Pylonepheritis pneumonia liver abscesss MI PE
•LUQ -PUD, Gastritis, GURD Hiatal hernia strangulated hiatal hernia, perforated Gastric ulcer, spleenic abscess, pylonephphritis, MI
•RLQ-Appendicitis, mesenteric lymphadenitis, caecal diverticulis mikel’s diverticulum
•LLQ- diverticulitis sigmoid vulvolus colon cancer nephro-lithiasis IBD torsion of ovarian cyst, PID ectopic pregnacy

Epigastric- Perf DU , Pancreatitis , Reflux, Gastritis, Ischemic bowel

33
Q

How is acute abdomen and surgical abdomen managed

A

management
•MEDICAL – Antibiotics, IVFs, Analgesia

  • All surgical abdomen would require an operation to resolve.
  • Operate or referred once the decision has been made the acute abdomen is surgical.
34
Q

How do you resuscitate

A
Resuscitate
•IVF
•NG tube
•Urine catheter
( end points of resuscitation)  optimization for surgery.
  • Analgesia
  • Broad spectrum antibiotics

•Resolve electrolyte imbalance
Exploratory laparotomy

35
Q

What is exploratory laparotomy

A

Exploratory laparotomy

•A relook at the patient- (Not a sign of weakness.)
this may be Mandatory or on Demand

Watch out for sepsis
Manage this using the survival sepsis guidelines

36
Q

What is the absolute figure for urine output in adults
Minimum urine output in an adult everyday and kids
Name three drugs that cause
Hameorhage
Name two markers for Coagulation

A

500 mls per day

1 ml per hour for adults
0.5 ml per hour for kids
8-9 liters of blood in a normal adult

Clexane
Aspirin
Warfarin
Anticoagulants

D dimer
Fibrinogen
FDPs