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Hepatic insufficiency
Chapter 13
Hepatic insufficiency Introduction
Insufficiency and congestion
The liver is the most multifaceted organ in the body. Preserving and optimizing its function should be a key consideration for the physician. The current biomechanical approach considers the liver as diseased only when there are gross histopathological or biomarker abnormalities, such as elevated liver enzymes, fibrosis, or hyperammonemia. In this approach, liver disease is primarily intrinsic liver disease, with little regard to the liver’s role in other disorders. In clinical Endobiogeny, the liver is integrated into the notion of precritical and critical terrains of many disorders. This broader view arises from the categorization of hepatic function into five broad categories, which link it to systemic function: (1) Metabolism, (2) Emunctory (detoxification, drainage), (3) Exocrine activity, (4) Endocrine activity, and (5) Adaptation. The first four ensure the fifth. We find that the liver is implicated in or affected by the neuroendocrine regulators of terrain, thus proper management of liver function will favorably affect the general regulation of the terrain, directly and indirectly (Table 13.1). This chapter presents a brief review of key concepts, symptoms, signs, and Biology of Function indexes related to the liver. A full discussion can be found in The Theory of Endobiogeny, Volume 2, Chapter 7.
Hepatic insufficiency is the inability of the liver to perform some function(s) at the level and/or duration demanded of it. Insufficiency can be relative or absolute (Table 13.2). Congestion is a response to insufficiency. Passive congestion occurs by increased inflow of blood. This increases the rate of material to be processed by the liver per second. Active congestion occurs by decreased outflow of blood to prolong the duration of exposure of material to hepatocytes. In a first time, congestion is adaptive, as it adapts the performance of the liver to demand. It becomes adaptative when it persists beyond its optimal time. This is why liver drainage is so important. A complete drainage of the liver may be sufficient in some cases to prevent exacerbation of disease or install a true cure.
General overview of function The liver is estimated to have over 500 known functions. Key activities are summarized in Table 13.3.
TABLE 13.1 Relationship of the liver to elements of the terrain. Terrain a
Metabolism
ANS
•
Corticotropic
•
Gonadotropic
•
Thyrotropic
•
Somatotropic
•
Immunity
•
Emunctory
Exocrine
•
Endocrine
Adaptation
•b
•
b
•
•b
• •
•
c
•
•d
a
Regulates rate of hepatic function and plays role in congestion. Indirect through production of binding globulins and carrier proteins. Direct: produces insulin-like growth factor. d Direct: produces thrombopoietin (platelet production). b c
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00013-5 © 2020 Elsevier Inc. All rights reserved.
111
112 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 13.2 Relative and absolute hepatic insufficiency. Hepatic insufficiency
System demand
Hepatic response
Example
Relative
Excessive
Insufficient for intensity
Prolonged Excessive and prolonged
Insufficient for duration Insufficient for intensity and duration
Adolescent growth phase after delayed linear growth, increased demand for insulin-like growth factors Chronic inflammation Chronic menometrorrhagia: 24-day cycle, 10 days of bleeding per cycle for multiple years
Appropriate
Insufficient
Absolute
TABLE 13.3 Overview of functions of the liver. Process
Subprocess
Examples
Metabolism
Carbohydrate storage and regulation Lipid storage and regulation Vitamin production
Neoglucogenesis Glycogenesis Glycogenolysis Lipogenesis Lipolysis Fat soluble: A, D, K Water soluble: B12, Iron, Copper Immunoglobulins Hormone carrier proteins Clotting factors Complement proteins Bile Cholesterol synthesis: cell wall, adrenal cortex, gonadal hormones
Protein production
Lipid production
Processing
Detoxification
Preparation for hematogenous distribution
Endocrine
Preparation for excretion
Circulating products Hormones Inflammatory proteins, etc.
Corticotropic
Angiotensin Cortisol-binding globulin Sex-hormone-binding globulin Vitamin D (intermediate metabolism) Insulin-like growth factors Platelet growth factor
Gonadotropic Thyrotropic Somatotropic Other Exocrine Adaptation
Waste products of cellular metabolism Ammonia → Urea Erythrocytes → Bilirubin Toxins Nutrients from alimentation
Excretion of products
All factors noted above Integration of all processes above
Pre-spring cleansing in the face of chronic hepatic vascular congestion
Units of function The liver has very little intrinsic metabolism for its own purposes. Most of its activity is in service of local, regional, and systemic demands. Optimal performance requires timed, sequential, and qualitative coordination with other organs related to it anatomically or functionally. This leads to the concept of “blocks” or grouped units of function: 1. Hepatobiliary: a. Anatomy: Gallbladder touches posterior aspect of liver; hepatic bile flows into gallbladder. b. Role: Creation, refinement, storage, excretion of bile—timed and proportional for: c. Effects: (1) Intestinal motricity (c.f. constipation), (2) Intestinal flora regulation (c.f. dysbiosis), (3) Nutrition: solubilization of fats. d. Exemplary plants: Carduus marianus, Taraxacum officinale. 2. Hepatobiliary-pancreatic: a. Anatomy: Exocrine pancreatic ducts merge with the common bile duct in the ampulla of Vater. The sphincter of Oddi allows of bile, bicarbonate and enzymes into the small intestines. Insufficient of one can lead to a delay of excretion of the other’s products. b. Role: Timed and proportional excretion of bile and digestive enzymes. c. Effects: Implicates liver in functioning of salivary glands, tonsils, lymph nodes, etc. d. Exemplary plants: Agrimonia eupatoria, Plantago major. It should be noted that many plants that work on the hepatobiliary-pancreatic unit do not drain the pancreas (c.f. Chapter 14: Exocrine pancreatic insufficiency). Rather, these plants have three categories of action: (1) hepatobiliary drainage, (2) stimulation of production of exocrine products (viz. bile, enzymes), and (3) substitutive action—this particularly refers to enzyme-like activity. This last a ction
Hepatic insufficiency Chapter | 13 113
is thought to allow the exocrine pancreas to increase the production and storage of endogenous enzymes over time, allowing for a reintegration of exocrine pancreatic function into digestion and adaptation. Because the portal vein takes all intestinally absorbed nutrition to the liver before systemic circulation, the liver is also implicated in functioning of other viscera through direct or indirect coupling, with clinical implications: 3. Hepato-gastric: a. Implication: Impaired regulation of mucosal surface. b. Exemplary plant: Achillea millefolium. 4. Hepato-intestinal: a. Implication: Impaired nutrient absorption, intestinal permeability (leaky gut). b. Exemplary plant: Plantago major. 5. Hepato-splenic: a. Implication: Impaired immunity and adaptability. b. Exemplary plant: Ceanothus americanus. 6. Hepato-splanchnic: a. Implications: All of the above to varying degrees. b. Exemplary plant: Anthemis nobilis, Carduus marianus. Thus, the notion of hepatic drainage often must be expanded to include the other associated units of function. This is determined by history and examination (following section). When in doubt, drain the hepatobiliary- pancreatic unit, unless other specific units of dysfunction are indicated.
Historical findings related to functional exocrine hepatic insufficiency There are numerous signs related to hepatic insufficiency. One can consider them with respect to post-prandial response to food (Table 13.4), hepatobiliary dysfunction (cholestasis) (Table 13.5), and the liver’s relationship to parasympathetic activity in response to the processing of foods (Table 13.6).
TABLE 13.4 Post-prandial signs. Symptom
Explanation
Comment
Post-prandial cold
Ears, tip of nose, digits
Active congestion αΣ > πΣ
Post-prandial heat
Warm ears
Passive congestion αΣ + histamines
Post-prandial flushing
Chest, abdomen
Passive congestion by βΣ
In response to carbohydrates: fatigue, heat
Impaired carbohydrate metabolism
In response to lipids: fatigue, gastric reflux, weight loss
Insufficient of lipid metabolism
Delayed wound healing
Insufficient protein metabolism
αΣ implicated in reflux
TABLE 13.5 Symptoms of cholestasis. Symptom
Explanation
Pruritis
Increased bile acids in serum and tissue
Stool changes
Poorly formed Odiferous (+ dysbiosis) Pale (insufficient bile salts) Fatty (Steatorrhea: insufficient bile salts)
Urinary changes
Dark color: increased bilirubin metabolites
Physical exam findings Numerous signs can be noted on examination of the head and mouth. Or, one may focus on the abdomen. Pain on palpation of the liver, gallbladder, and exocrine pancreas is significant for edema of the physical organ or, a signification via its projection point (Fig. 13.1). There are a number of signs related to exocrine hepatic insufficiency: 1. Cholestasis (listed from head to abdomen) a. Icterus b. Edema of inferior eyelids
TABLE 13.6 Relaunching parasympathetic activity. Symptom Post-prandial fatigue Post-prandial sweating Sweating during sleep Hypersialorrhea while falling asleep Hypersialorrhea during sleep
114 SECTION | B Essentials of history, physical exam and Biology of Functions
c. Halitosis d. Coating on tongue e. Hepatomegaly 2. Splanchnic congestion (listed from head to abdomen) a. Relative neutropenia due to hepatic sequestration b. Spider (stellate) nevi: face, nose, eyelids, vena cava c. Varicose veins: Palate, thorax d. Icteric velum (soft palate) e. Thenar and hypothenar palmar erythema f. Subcutaneous tissue congestion in the peri-hepatic zone (Fig. 13.1) g. Hepatomegaly 3. Sphincter of Oddi a. Sensitive to palpation (Fig. 13.1) 4. Autonomic disturbance a. Lower arterial blood pressure than anticipated b. Sleep-wake cycle: Diurnal somnolence with waking at the end of the night
Liver congestion: Secretory
Liver congestion: Circulatory
Biology of Function indices related to Hepatic insufficiency Hepatic insufficiency is best determined by history and physical examination. Three indexes relate in part to hepato- splanchnic dysfunction. The first is Leukocyte mobilization index (LMI), which expresses the liberating capacity of leukocyte sequestered in the splanchnic vs. hepatic space. The second is Platelet mobilization index (PMI), which expresses the liberating capacity of platelets sequestered in the splanchnic vs. splenic space (Table 13.7). A dysfunction in their relationships installs a latent spasmophilia (Table 13.8, and Theory of Endobiogeny Volume 2, Chapter 11: Spasmophilia). The third is the Starter index, which is the ratio LMI÷PMI. It evaluates three levels of function: (1) liver vs. spleen for immune cells in adaptation (leukocytes vs. platelets), (2) glucagon (endocrine pancreas) vs. adrenaline (liver), (3) TRH-Glucagon vs. Alpha-Cortisol.
Splanchnic congestion® hepato-pancreatic blockage
Zone of distress Murphy’s Point: Congestion: Sphincter of Oddi
Hepatic congestion, extra-hepatic: Sphincter of Oddi, Splanchnic congestion, Duodenal plexus
Endocrine pancreas overtaxed General pancreatic congestion Exocrine pancreatic congestion
FIG. 13.1 Anterior abdominal findings related to the liver and other viscera. According to the theory of Endobiogeny, there are direct anatomical points of palpation (liver: metabolic and circulatory congestion) and projections onto the abdominal surface (all other points in this diagram). All points are elicited by deep and firm palpation except extrahepatic zone of congestion and zone of distress. These are determined by light palpation. The zone of distress refers to splenic congestion related to grief and distress and a latent state of physiologic depression. Modified and used with permission from an original drawing by Duraffourd and Lapraz, unpublished.
Hepatic insufficiency Chapter | 13 115
TABLE 13.7 Interpretation of Leukocyte and Platelet mobilization indexes. Index
Factor
High
Low
LMI
Alpha Leukocyte source
Adaptive alpha Splanchnic > hepatic
Adaptative alpha Hepatic > splanchnic Vascular hepatic congestion due to solicitation of splanchnic bed for adaptation
PMI
Beta Platelet source
Prominent beta Splanchnic > splenic
Beta blocked Splenic > splanchnic Metabolic hepatic congestion: reliance on de novo platelets in bone marrow by thrombopoietin
LMI, Leukocyte mobilization index; PMI, Platelet mobilization index.
TABLE 13.8 Interpretation of Leukocyte and Platelet mobilization indexes in relationship to one another. LMI
PMI
Interpretation
↑
↑
General sympathetic activity increased on splanchnic bed
↑
↔
Delayed beta, favors spasmophilia
↑
↓
Blocked beta, favors spasmophilia
↓
↓
Adaptative hyper-alpha with blocked beta, favors hepato-splenic congestion
Therapeutics: General considerations The therapeutic approach to hepatic insufficiency involves a rational clinical determination of two questions. The first is: What other organs, systems or processes are also implicated? This will influence the type of plant selected. Example: 4-year-old with recurrent pharyngitis: On history: post-prandial heat when eating sugary foods (liver), on exam: coating on the tongue (cholestasis), dilated opening of canal of Stensen (exocrine pancreas). Conclusion: hepatobiliary-pancreatic unit implicated. Plant: Plantago major: treats the entire block as well as tropism for ear, nose, and throat area, immunomodulation and antimicrobial activity.
The second question is: Is the hepatic dysfunction precritical, critical, or, both, and, what aspect of liver dysfunction is implicated? Example: Crohn’s disease: The liver is primarily implicated in the critical terrain because of its role in adaptation
and processing inflammatory proteins. So, primary drainage of the liver is during the critical state, not the precritical state. In the critical state of a Crohn’s flare up, the liver drainer should be somewhat strong and rapid in action, such as Taraxacum officinale or Cynara scolymus.
Conclusions The liver plays a critical role in health and thus in illness. Long before gross liver histopathology, there is hepatic insufficiency, which brings about an adaptative congestion, which necessitates drainage. The Endobiogenic approach to liver support involves the selection of medicinal plants, oligoelements, and foods that address (1) intrinsic hepatic activity, (2) its functional and anatomical relationship to other organs, (3) its implication in disease with specificity to precritical or critical terrain. History and physical examination are the primary methods of determining evaluating the liver and its role in disbalance. This allows for a rational, clinical selection of the optimal approach to supporting the liver.
Hepatic insufficiency Introduction
Insufficiency and congestion
The liver is the most multifaceted organ in the body. Preserving and optimizing its function should be a key consideration for the physician. The current biomechanical approach considers the liver as diseased only when there are gross histopathological or biomarker abnormalities, such as elevated liver enzymes, fibrosis, or hyperammonemia. In this approach, liver disease is primarily intrinsic liver disease, with little regard to the liver’s role in other disorders. In clinical Endobiogeny, the liver is integrated into the notion of precritical and critical terrains of many disorders. This broader view arises from the categorization of hepatic function into five broad categories, which link it to systemic function: (1) Metabolism, (2) Emunctory (detoxification, drainage), (3) Exocrine activity, (4) Endocrine activity, and (5) Adaptation. The first four ensure the fifth. We find that the liver is implicated in or affected by the neuroendocrine regulators of terrain, thus proper management of liver function will favorably affect the general regulation of the terrain, directly and indirectly (Table 13.1). This chapter presents a brief review of key concepts, symptoms, signs, and Biology of Function indexes related to the liver. A full discussion can be found in The Theory of Endobiogeny, Volume 2, Chapter 7.
Hepatic insufficiency is the inability of the liver to perform some function(s) at the level and/or duration demanded of it. Insufficiency can be relative or absolute (Table 13.2). Congestion is a response to insufficiency. Passive congestion occurs by increased inflow of blood. This increases the rate of material to be processed by the liver per second. Active congestion occurs by decreased outflow of blood to prolong the duration of exposure of material to hepatocytes. In a first time, congestion is adaptive, as it adapts the performance of the liver to demand. It becomes adaptative when it persists beyond its optimal time. This is why liver drainage is so important. A complete drainage of the liver may be sufficient in some cases to prevent exacerbation of disease or install a true cure.
General overview of function The liver is estimated to have over 500 known functions. Key activities are summarized in Table 13.3.
TABLE 13.1 Relationship of the liver to elements of the terrain. Terrain a
Metabolism
ANS
•
Corticotropic
•
Gonadotropic
•
Thyrotropic
•
Somatotropic
•
Immunity
•
Emunctory
Exocrine
•
Endocrine
Adaptation
•b
•
b
•
•b
• •
•
c
•
•d
a
Regulates rate of hepatic function and plays role in congestion. Indirect through production of binding globulins and carrier proteins. Direct: produces insulin-like growth factor. d Direct: produces thrombopoietin (platelet production). b c
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00013-5 © 2020 Elsevier Inc. All rights reserved.
111
112 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 13.2 Relative and absolute hepatic insufficiency. Hepatic insufficiency
System demand
Hepatic response
Example
Relative
Excessive
Insufficient for intensity
Prolonged Excessive and prolonged
Insufficient for duration Insufficient for intensity and duration
Adolescent growth phase after delayed linear growth, increased demand for insulin-like growth factors Chronic inflammation Chronic menometrorrhagia: 24-day cycle, 10 days of bleeding per cycle for multiple years
Appropriate
Insufficient
Absolute
TABLE 13.3 Overview of functions of the liver. Process
Subprocess
Examples
Metabolism
Carbohydrate storage and regulation Lipid storage and regulation Vitamin production
Neoglucogenesis Glycogenesis Glycogenolysis Lipogenesis Lipolysis Fat soluble: A, D, K Water soluble: B12, Iron, Copper Immunoglobulins Hormone carrier proteins Clotting factors Complement proteins Bile Cholesterol synthesis: cell wall, adrenal cortex, gonadal hormones
Protein production
Lipid production
Processing
Detoxification
Preparation for hematogenous distribution
Endocrine
Preparation for excretion
Circulating products Hormones Inflammatory proteins, etc.
Corticotropic
Angiotensin Cortisol-binding globulin Sex-hormone-binding globulin Vitamin D (intermediate metabolism) Insulin-like growth factors Platelet growth factor
Gonadotropic Thyrotropic Somatotropic Other Exocrine Adaptation
Waste products of cellular metabolism Ammonia → Urea Erythrocytes → Bilirubin Toxins Nutrients from alimentation
Excretion of products
All factors noted above Integration of all processes above
Pre-spring cleansing in the face of chronic hepatic vascular congestion
Units of function The liver has very little intrinsic metabolism for its own purposes. Most of its activity is in service of local, regional, and systemic demands. Optimal performance requires timed, sequential, and qualitative coordination with other organs related to it anatomically or functionally. This leads to the concept of “blocks” or grouped units of function: 1. Hepatobiliary: a. Anatomy: Gallbladder touches posterior aspect of liver; hepatic bile flows into gallbladder. b. Role: Creation, refinement, storage, excretion of bile—timed and proportional for: c. Effects: (1) Intestinal motricity (c.f. constipation), (2) Intestinal flora regulation (c.f. dysbiosis), (3) Nutrition: solubilization of fats. d. Exemplary plants: Carduus marianus, Taraxacum officinale. 2. Hepatobiliary-pancreatic: a. Anatomy: Exocrine pancreatic ducts merge with the common bile duct in the ampulla of Vater. The sphincter of Oddi allows of bile, bicarbonate and enzymes into the small intestines. Insufficient of one can lead to a delay of excretion of the other’s products. b. Role: Timed and proportional excretion of bile and digestive enzymes. c. Effects: Implicates liver in functioning of salivary glands, tonsils, lymph nodes, etc. d. Exemplary plants: Agrimonia eupatoria, Plantago major. It should be noted that many plants that work on the hepatobiliary-pancreatic unit do not drain the pancreas (c.f. Chapter 14: Exocrine pancreatic insufficiency). Rather, these plants have three categories of action: (1) hepatobiliary drainage, (2) stimulation of production of exocrine products (viz. bile, enzymes), and (3) substitutive action—this particularly refers to enzyme-like activity. This last a ction
Hepatic insufficiency Chapter | 13 113
is thought to allow the exocrine pancreas to increase the production and storage of endogenous enzymes over time, allowing for a reintegration of exocrine pancreatic function into digestion and adaptation. Because the portal vein takes all intestinally absorbed nutrition to the liver before systemic circulation, the liver is also implicated in functioning of other viscera through direct or indirect coupling, with clinical implications: 3. Hepato-gastric: a. Implication: Impaired regulation of mucosal surface. b. Exemplary plant: Achillea millefolium. 4. Hepato-intestinal: a. Implication: Impaired nutrient absorption, intestinal permeability (leaky gut). b. Exemplary plant: Plantago major. 5. Hepato-splenic: a. Implication: Impaired immunity and adaptability. b. Exemplary plant: Ceanothus americanus. 6. Hepato-splanchnic: a. Implications: All of the above to varying degrees. b. Exemplary plant: Anthemis nobilis, Carduus marianus. Thus, the notion of hepatic drainage often must be expanded to include the other associated units of function. This is determined by history and examination (following section). When in doubt, drain the hepatobiliary- pancreatic unit, unless other specific units of dysfunction are indicated.
Historical findings related to functional exocrine hepatic insufficiency There are numerous signs related to hepatic insufficiency. One can consider them with respect to post-prandial response to food (Table 13.4), hepatobiliary dysfunction (cholestasis) (Table 13.5), and the liver’s relationship to parasympathetic activity in response to the processing of foods (Table 13.6).
TABLE 13.4 Post-prandial signs. Symptom
Explanation
Comment
Post-prandial cold
Ears, tip of nose, digits
Active congestion αΣ > πΣ
Post-prandial heat
Warm ears
Passive congestion αΣ + histamines
Post-prandial flushing
Chest, abdomen
Passive congestion by βΣ
In response to carbohydrates: fatigue, heat
Impaired carbohydrate metabolism
In response to lipids: fatigue, gastric reflux, weight loss
Insufficient of lipid metabolism
Delayed wound healing
Insufficient protein metabolism
αΣ implicated in reflux
TABLE 13.5 Symptoms of cholestasis. Symptom
Explanation
Pruritis
Increased bile acids in serum and tissue
Stool changes
Poorly formed Odiferous (+ dysbiosis) Pale (insufficient bile salts) Fatty (Steatorrhea: insufficient bile salts)
Urinary changes
Dark color: increased bilirubin metabolites
Physical exam findings Numerous signs can be noted on examination of the head and mouth. Or, one may focus on the abdomen. Pain on palpation of the liver, gallbladder, and exocrine pancreas is significant for edema of the physical organ or, a signification via its projection point (Fig. 13.1). There are a number of signs related to exocrine hepatic insufficiency: 1. Cholestasis (listed from head to abdomen) a. Icterus b. Edema of inferior eyelids
TABLE 13.6 Relaunching parasympathetic activity. Symptom Post-prandial fatigue Post-prandial sweating Sweating during sleep Hypersialorrhea while falling asleep Hypersialorrhea during sleep
114 SECTION | B Essentials of history, physical exam and Biology of Functions
c. Halitosis d. Coating on tongue e. Hepatomegaly 2. Splanchnic congestion (listed from head to abdomen) a. Relative neutropenia due to hepatic sequestration b. Spider (stellate) nevi: face, nose, eyelids, vena cava c. Varicose veins: Palate, thorax d. Icteric velum (soft palate) e. Thenar and hypothenar palmar erythema f. Subcutaneous tissue congestion in the peri-hepatic zone (Fig. 13.1) g. Hepatomegaly 3. Sphincter of Oddi a. Sensitive to palpation (Fig. 13.1) 4. Autonomic disturbance a. Lower arterial blood pressure than anticipated b. Sleep-wake cycle: Diurnal somnolence with waking at the end of the night
Liver congestion: Secretory
Liver congestion: Circulatory
Biology of Function indices related to Hepatic insufficiency Hepatic insufficiency is best determined by history and physical examination. Three indexes relate in part to hepato- splanchnic dysfunction. The first is Leukocyte mobilization index (LMI), which expresses the liberating capacity of leukocyte sequestered in the splanchnic vs. hepatic space. The second is Platelet mobilization index (PMI), which expresses the liberating capacity of platelets sequestered in the splanchnic vs. splenic space (Table 13.7). A dysfunction in their relationships installs a latent spasmophilia (Table 13.8, and Theory of Endobiogeny Volume 2, Chapter 11: Spasmophilia). The third is the Starter index, which is the ratio LMI÷PMI. It evaluates three levels of function: (1) liver vs. spleen for immune cells in adaptation (leukocytes vs. platelets), (2) glucagon (endocrine pancreas) vs. adrenaline (liver), (3) TRH-Glucagon vs. Alpha-Cortisol.
Splanchnic congestion® hepato-pancreatic blockage
Zone of distress Murphy’s Point: Congestion: Sphincter of Oddi
Hepatic congestion, extra-hepatic: Sphincter of Oddi, Splanchnic congestion, Duodenal plexus
Endocrine pancreas overtaxed General pancreatic congestion Exocrine pancreatic congestion
FIG. 13.1 Anterior abdominal findings related to the liver and other viscera. According to the theory of Endobiogeny, there are direct anatomical points of palpation (liver: metabolic and circulatory congestion) and projections onto the abdominal surface (all other points in this diagram). All points are elicited by deep and firm palpation except extrahepatic zone of congestion and zone of distress. These are determined by light palpation. The zone of distress refers to splenic congestion related to grief and distress and a latent state of physiologic depression. Modified and used with permission from an original drawing by Duraffourd and Lapraz, unpublished.
Hepatic insufficiency Chapter | 13 115
TABLE 13.7 Interpretation of Leukocyte and Platelet mobilization indexes. Index
Factor
High
Low
LMI
Alpha Leukocyte source
Adaptive alpha Splanchnic > hepatic
Adaptative alpha Hepatic > splanchnic Vascular hepatic congestion due to solicitation of splanchnic bed for adaptation
PMI
Beta Platelet source
Prominent beta Splanchnic > splenic
Beta blocked Splenic > splanchnic Metabolic hepatic congestion: reliance on de novo platelets in bone marrow by thrombopoietin
LMI, Leukocyte mobilization index; PMI, Platelet mobilization index.
TABLE 13.8 Interpretation of Leukocyte and Platelet mobilization indexes in relationship to one another. LMI
PMI
Interpretation
↑
↑
General sympathetic activity increased on splanchnic bed
↑
↔
Delayed beta, favors spasmophilia
↑
↓
Blocked beta, favors spasmophilia
↓
↓
Adaptative hyper-alpha with blocked beta, favors hepato-splenic congestion
Therapeutics: General considerations The therapeutic approach to hepatic insufficiency involves a rational clinical determination of two questions. The first is: What other organs, systems or processes are also implicated? This will influence the type of plant selected. Example: 4-year-old with recurrent pharyngitis: On history: post-prandial heat when eating sugary foods (liver), on exam: coating on the tongue (cholestasis), dilated opening of canal of Stensen (exocrine pancreas). Conclusion: hepatobiliary-pancreatic unit implicated. Plant: Plantago major: treats the entire block as well as tropism for ear, nose, and throat area, immunomodulation and antimicrobial activity.
The second question is: Is the hepatic dysfunction precritical, critical, or, both, and, what aspect of liver dysfunction is implicated? Example: Crohn’s disease: The liver is primarily implicated in the critical terrain because of its role in adaptation
and processing inflammatory proteins. So, primary drainage of the liver is during the critical state, not the precritical state. In the critical state of a Crohn’s flare up, the liver drainer should be somewhat strong and rapid in action, such as Taraxacum officinale or Cynara scolymus.
Conclusions The liver plays a critical role in health and thus in illness. Long before gross liver histopathology, there is hepatic insufficiency, which brings about an adaptative congestion, which necessitates drainage. The Endobiogenic approach to liver support involves the selection of medicinal plants, oligoelements, and foods that address (1) intrinsic hepatic activity, (2) its functional and anatomical relationship to other organs, (3) its implication in disease with specificity to precritical or critical terrain. History and physical examination are the primary methods of determining evaluating the liver and its role in disbalance. This allows for a rational, clinical selection of the optimal approach to supporting the liver.